Edit count of the user (user_editcount) | null |
Name of the user account (user_name) | '2A02:C7E:EC9:3C00:C113:9014:935A:89E0' |
Age of the user account (user_age) | 0 |
Groups (including implicit) the user is in (user_groups) | [
0 => '*'
] |
Rights that the user has (user_rights) | [
0 => 'createaccount',
1 => 'read',
2 => 'edit',
3 => 'createtalk',
4 => 'writeapi',
5 => 'viewmywatchlist',
6 => 'editmywatchlist',
7 => 'viewmyprivateinfo',
8 => 'editmyprivateinfo',
9 => 'editmyoptions',
10 => 'abusefilter-log-detail',
11 => 'urlshortener-create-url',
12 => 'centralauth-merge',
13 => 'abusefilter-view',
14 => 'abusefilter-log',
15 => 'vipsscaler-test'
] |
Whether the user is blocked (user_blocked) | false |
Whether the user is editing from mobile app (user_app) | false |
Whether or not a user is editing through the mobile interface (user_mobile) | false |
Page ID (page_id) | 443416 |
Page namespace (page_namespace) | 0 |
Page title without namespace (page_title) | 'Phagocyte' |
Full page title (page_prefixedtitle) | 'Phagocyte' |
Edit protection level of the page (page_restrictions_edit) | [] |
Last ten users to contribute to the page (page_recent_contributors) | [
0 => 'Headbomb',
1 => 'LucasKannou',
2 => '174.102.139.84',
3 => 'Pulpfiction621',
4 => 'Citation bot',
5 => 'LR0725',
6 => 'Graham Beards',
7 => 'ClueBot NG',
8 => 'Dhitshisturber',
9 => 'BiomedStudent12'
] |
Page age in seconds (page_age) | 589759003 |
Action (action) | 'edit' |
Edit summary/reason (summary) | '' |
Old content model (old_content_model) | 'wikitext' |
New content model (new_content_model) | 'wikitext' |
Old page wikitext, before the edit (old_wikitext) | '{{pp-move-indef}}
{{short description|Cells that ingest harmful matter within the body}}
{{Use mdy dates|date=November 2021}}
[[File:Neutrophil with anthrax copy.jpg|thumb|[[Scanning electron microscope|Scanning electron micrograph]] of a [[Neutrophil granulocyte|neutrophil]] phagocytosing [[Bacillus anthracis|anthrax bacilli]] (orange)|alt= Long rod-shaped bacteria, one of which has been partially engulfed by a larger blob-shaped white blood cell. The shape of the cell is distorted by undigested bacterium inside it.]]
'''Phagocytes''' are [[cell (biology)|cell]]s that protect the body by ingesting harmful foreign particles, [[bacteria]], and dead or [[Apoptosis|dying]] cells. Their name comes from the [[Greek language|Greek]] ''{{lang|grc-Latn|phagein}}'', "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek ''kutos'', "hollow vessel".<ref name=ox>{{cite book|authors=Little, C., Fowler H.W., Coulson J.| title=The Shorter Oxford English Dictionary| publisher=Oxford University Press (Guild Publishing)| year=1983|pages=1566–67}}</ref> They are essential for fighting infections and for subsequent [[immunity (medical)|immunity]].<ref name=USC>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=2–10}}</ref> Phagocytes are important throughout the animal kingdom<ref name=Delves250>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=250}}</ref> and are highly developed within vertebrates.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=251}}</ref> One [[litre]] of human blood contains about six billion phagocytes.<ref name=Hoff-values>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=331}}</ref> They were discovered in 1882 by [[Élie Metchnikoff|Ilya Ilyich Mechnikov]] while he was studying [[starfish]] [[larva]]e.<ref name= Ilya>[http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html Ilya Mechnikov], retrieved on November 28, 2008. From [http://nobelprize.org/nobelfoundation/publications/lectures/index.html Nobel Lectures], ''Physiology or Medicine 1901–1921'', Elsevier Publishing Company, Amsterdam, 1967. {{webarchive |url=https://web.archive.org/web/20080822041214/http://nobelprize.org/nobelfoundation/publications/lectures/index.html |date=August 22, 2008 }}</ref> Mechnikov was awarded the 1908 [[Nobel Prize in Physiology or Medicine]] for his discovery.<ref name=Paul>{{cite journal|title=Ilya Ilich Metchnikoff (1845–1915) and Paul Ehrlich (1854–1915): the centennial of the 1908 Nobel Prize in Physiology or Medicine|journal=Journal of Medical Biography|year=2008|first=FC|last=Schmalstieg|author2=AS Goldman|volume=16|issue=2|pages=96–103|pmid=18463079|doi=10.1258/jmb.2008.008006|s2cid=25063709}}</ref> Phagocytes occur in many species; some [[amoeboid|amoebae]] behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.<ref name=amoebaphage>Janeway, Chapter: [https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=phagocytes,evolution&rid=imm.section.2367#2368 Evolution of the innate immune system.] retrieved on March 20, 2009</ref>
Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at [[phagocytosis]].<ref name=Ernst186>{{Harvnb|Ernst|Stendahl|2006|p=186}}</ref> The professional phagocytes include many types of [[white blood cell]]s (such as [[neutrophil]]s, [[monocyte]]s, [[macrophage]]s, [[mast cell]]s, and [[dendritic cell]]s).<ref name=Rob>{{Harvnb|Robinson|Babcock|1998|p=187}} and {{Harvnb|Ernst|Stendahl|2006|pp=7–10}}</ref> The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called [[receptor (biochemistry)|receptors]] on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body.<ref name= something>{{Harvnb|Ernst|Stendahl|2006|p=10}}</ref> Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan.<ref name="pathogenesis"/>
During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called [[chemotaxis]]. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte.<ref name=money/> Some phagocytes kill the ingested pathogen with [[reactive oxygen species|oxidants]] and [[nitric oxide]].<ref name=pmid15378046>{{cite journal |author=Fang FC |title=Antimicrobial reactive oxygen and nitrogen species: concepts and controversies |journal=Nat. Rev. Microbiol. |volume=2 |issue=10 |pages=820–32 |date=October 2004 |pmid=15378046 |doi=10.1038/nrmicro1004 |s2cid=11063073 }}</ref> After phagocytosis, macrophages and dendritic cells can also participate in [[antigen presentation]], a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's [[lymph node]]s and display the material to white blood cells called [[lymphocytes]]. This process is important in building immunity,<ref name=ATP>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=172–84}}</ref> and many pathogens have evolved methods to evade attacks by phagocytes.<ref name=USC/>
== History ==
[[File:Professeur Metchnikoff, portrait du scientifique dans un laboratoire de recherche.jpg|thumb|Ilya Ilyich Mechnikov in his laboratory|alt=A bearded old man holding up a test tube. He is sitting at a table by a window. The table is covered with many small bottles and test tubes.]]
The Russian zoologist [[Ilya Ilyich Mechnikov]] (1845–1916) first recognized that specialized cells were involved in defense against microbial infections.<ref name="pmid31001278">{{cite journal |vauthors=Kaufmann SH|title=Immunology's Coming of Age |journal=Frontiers in Immunology |volume=10 |pages=684 |date=2019 |pmid=31001278 |pmc=6456699 |doi=10.3389/fimmu.2019.00684 |doi-access=free }}</ref> In 1882, he studied [[motility|motile]] (freely moving) cells in the [[larva]]e of [[Sea star|starfishes]], believing they were important to the animals' immune defenses. To test his idea, he inserted small thorns from a [[tangerine]] tree into the larvae. After a few hours he noticed that the motile cells had surrounded the thorns.<ref name="pmid31001278"/> Mechnikov traveled to [[Vienna]] and shared his ideas with [[Carl Friedrich Wilhelm Claus|Carl Friedrich Claus]] who suggested the name "phagocyte" (from the Greek words ''{{lang|grc-Latn|phagein}}'', meaning "to eat or devour", and ''{{lang|grc-Latn|kutos}}'', meaning "hollow vessel"<ref name=ox />) for the cells that Mechnikov had observed.<ref name="pmid9544583">{{cite journal | author = Aterman K | title = Medals, memoirs—and Metchnikoff | journal = J. Leukoc. Biol. | volume = 63 | issue = 4 | pages = 515–17 | date = April 1, 1998 | pmid = 9544583 | doi = 10.1002/jlb.63.4.515 | s2cid = 44748502 | doi-access = free }}</ref>
A year later, Mechnikov studied a fresh water [[crustacean]] called ''[[Daphnia]]'', a tiny transparent animal that can be examined directly under a microscope. He discovered that fungal spores that attacked the animal were destroyed by phagocytes. He went on to extend his observations to the white blood cells of mammals and discovered that the bacterium ''[[Bacillus anthracis]]'' could be engulfed and killed by phagocytes, a process that he called [[phagocytosis]].<ref name=autogenerated5>{{cite web|url=http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html|title=Ilya Mechnikov|publisher=The Nobel Foundation|access-date=December 19, 2014}}</ref> Mechnikov proposed that phagocytes were a primary defense against invading organisms.<ref name="pmid31001278"/>
In 1903, [[Almroth Wright]] discovered that phagocytosis was reinforced by specific [[antibody|antibodies]] that he called [[opsonin]]s, from the Greek ''[[opson]]'', "a dressing or relish".<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=263}}</ref> Mechnikov was awarded (jointly with [[Paul Ehrlich]]) the 1908 [[Nobel Prize in Physiology or Medicine]] for his work on phagocytes and phagocytosis.<ref name= Paul/>
Although the importance of these discoveries slowly gained acceptance during the early twentieth century, the intricate relationships between phagocytes and all the other components of the immune system were not known until the 1980s.<ref>{{Harvnb|Robinson|Babcock|1998|p=vii}}</ref>
== Phagocytosis ==
{{main|Phagocytosis}}
[[File:Phagocytosis in three steps.png|thumb|Phagocytosis in three steps: 1. Unbound phagocyte surface receptors do not trigger phagocytosis. 2. Binding of receptors causes them to cluster. 3. Phagocytosis is triggered and the particle is taken up by the phagocyte.|alt=A cartoon: 1. The particle is depicted by an oval and the surface of the phagocyte by a straight line. Different smaller shapes are on the line and the oval. 2. The smaller particles on each surface join. 3. The line is now concave and partially wraps around the oval.]]
Phagocytosis is the process of taking in particles such as bacteria, invasive [[fungi]], parasites, [[apoptosis|dead host cells]], and cellular and foreign debris by a cell.<ref name=superman2>{{Harvnb|Ernst|Stendahl|2006|p=4}}</ref> It involves a chain of molecular processes.<ref>{{Harvnb|Ernst|Stendahl|2006|p=78}}</ref><ref name="pmid29727727">{{cite journal |vauthors=Feldman MB, Vyas JM, Mansour MK |title=It takes a village: Phagocytes play a central role in fungal immunity |journal=Seminars in Cell & Developmental Biology |volume=89 |issue= |pages=16–23 |date=May 2019 |pmid=29727727 |pmc=6235731 |doi=10.1016/j.semcdb.2018.04.008}}</ref> Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called "receptors" that are on the surface of the phagocyte. The phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes.<ref name="pmid8301210">{{cite journal | author = Hampton MB, Vissers MC, Winterbourn CC | title = A single assay for measuring the rates of phagocytosis and bacterial killing by neutrophils | journal = J. Leukoc. Biol. | volume = 55 | issue = 2 | pages = 147–52 | date = February 1994 | pmid = 8301210 | doi = 10.1002/jlb.55.2.147| url = http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210 | archive-url = https://archive.today/20121228084302/http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210 | url-status = dead | archive-date = December 28, 2012 | last2 = Vissers | last3 = Winterbourn | s2cid = 44911791 | access-date = December 19, 2014 }}</ref> Once inside this phagocyte, the bacterium is trapped in a compartment called a [[phagosome]]. Within one minute the phagosome merges with either a [[lysosome]] or a [[Granule (cell biology)|granule]] to form a [[phagolysosome]]. The bacterium is then subjected to an overwhelming array of killing mechanisms<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–7}}</ref> and is dead a few minutes later.<ref name="pmid8301210"/> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> Phagocytes have voracious appetites; scientists have even fed macrophages with [[iron filings]] and then used a small magnet to separate them from other cells.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref>
[[File:Opsonin.png|thumb|left|Macrophages have special receptors that enhance phagocytosis (not to scale)|alt=A cartoon: The macrophage is depicted as a distorted solid circle. On the surface of the circle is a small y-shaped figure that is connected to a solid rectangle that depicts a bacterium.]]
A phagocyte has many types of receptors on its surface that are used to bind material.<ref name=USC/> They include [[opsonin]] receptors, [[scavenger receptor (immunology)|scavenger receptor]]s, and [[Toll-like receptors]]. Opsonin receptors increase the phagocytosis of bacteria that have been coated with [[immunoglobulin G]] (IgG) [[antibodies]] or with [[complement system|complement]]. "Complement" is the name given to a complex series of protein molecules found in the blood that destroy cells or mark them for destruction.<ref>{{Harvnb|Sompayrac|2019|pp=13–16}}</ref> Scavenger receptors bind to a large range of molecules on the surface of bacterial cells, and Toll-like receptors—so called because of their similarity to well-studied receptors in fruit flies that are encoded by the [[Toll (gene)|Toll gene]]—bind to more specific molecules. Binding to Toll-like receptors increases phagocytosis and causes the phagocyte to release a group of hormones that cause [[inflammation]].<ref name=USC/>
== Methods of killing ==
[[File:Phagocytosis2.png|thumb|Simplified diagram of the phagocytosis and destruction of a bacterial cell|alt=A cartoon that depicts the engulfment of a single bacterium, its passage through a cell where it is digested and released as debris.]]
The killing of microbes is a critical function of phagocytes that is performed either within the phagocyte ([[intracellular]] killing) or outside of the phagocyte ([[extracellular]] killing).<ref name="pmid18684880">{{cite journal
| author = Dale DC, Boxer L, Liles WC
| title = The phagocytes: neutrophils and monocytes
| journal = Blood | volume = 112 | issue = 4 | pages = 935–45 |date=August 2008 | pmid = 18684880 | doi = 10.1182/blood-2007-12-077917 | last2 = Boxer
| last3 = Liles
| s2cid = 746699
| doi-access = free }}</ref>
=== Oxygen-dependent intracellular ===
When a phagocyte ingests bacteria (or any material), its oxygen consumption increases. The increase in oxygen consumption, called a [[respiratory burst]], produces reactive oxygen-containing molecules that are anti-microbial.<ref>{{cite journal|title=Respiratory burst in human neutrophils|journal=Journal of Immunological Methods|date=December 17, 1999|first=C|last=Dahlgren|author2=A Karlsson|volume=232|issue=1–2|pages=3–14|pmid=10618505|doi=10.1016/S0022-1759(99)00146-5}}</ref> The oxygen compounds are toxic to both the invader and the cell itself, so they are kept in compartments inside the cell. This method of killing invading microbes by using the reactive oxygen-containing molecules is referred to as oxygen-dependent intracellular killing, of which there are two types.<ref name = pmid15378046/>
The first type is the oxygen-dependent production of a [[superoxide]],<ref name=USC/> which is an oxygen-rich bacteria-killing substance.<ref>{{cite journal|title=NADPH oxidase|journal=The International Journal of Biochemistry & Cell Biology|year=1996|first=KP|last=Shatwell|author2=AW Segal|volume=28|issue=11|pages=1191–95|pmid=9022278|doi=10.1016/S1357-2725(96)00084-2}}</ref> The superoxide is converted to [[hydrogen peroxide]] and [[singlet oxygen]] by an enzyme called [[superoxide dismutase]]. Superoxides also react with the hydrogen peroxide to produce [[hydroxyl radicals]], which assist in killing the invading microbe.<ref name=USC/>
The second type involves the use of the enzyme [[myeloperoxidase]] from neutrophil granules.<ref name="pmid10519157">{{cite journal | author = Klebanoff SJ | title = Myeloperoxidase | journal = Proc. Assoc. Am. Physicians | volume = 111 | issue = 5 | pages = 383–89 | year = 1999 | pmid = 10519157 | doi = 10.1111/paa.1999.111.5.383}}</ref> When granules fuse with a phagosome, myeloperoxidase is released into the phagolysosome, and this enzyme uses hydrogen peroxide and [[chlorine]] to create [[hypochlorite]], a substance used in domestic [[bleach]]. Hypochlorite is extremely toxic to bacteria.<ref name=USC/> Myeloperoxidase contains a [[heme]] pigment, which accounts for the green color of secretions rich in neutrophils, such as [[pus]] and infected [[sputum]].<ref name="pmid15478278">{{cite journal | author = Meyer KC | title = Neutrophils, myeloperoxidase, and bronchiectasis in cystic fibrosis: green is not good | journal = J. Lab. Clin. Med. | volume = 144 | issue = 3 | pages = 124–26 |date=September 2004 | pmid = 15478278 | doi = 10.1016/j.lab.2004.05.014}}</ref>
=== Oxygen-independent intracellular ===
[[File:Gram-stain of gonorrhoea.jpg|thumb|right|Micrograph of [[Gram-stain]]ed [[pus]] showing ''[[Neisseria gonorrhoeae]]'' bacteria inside phagocytes and their relative sizes|alt=Pus under a microscope, there are many white blood cells with lobed nuclei. Inside some of the cells there are hundreds of bacteria that have been engulfed.]]
Phagocytes can also kill microbes by oxygen-independent methods, but these are not as effective as the oxygen-dependent ones. There are four main types. The first uses electrically charged proteins that damage the bacterium's [[cell membrane|membrane]]. The second type uses lysozymes; these enzymes break down the bacterial [[cell wall]]. The third type uses [[lactoferrin]]s, which are present in neutrophil granules and remove essential iron from bacteria.<ref>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=118}}</ref> The fourth type uses [[proteases]] and [[hydrolytic enzymes]]; these enzymes are used to digest the proteins of destroyed bacteria.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–10}}</ref>
=== Extracellular ===
[[Interferon-gamma]]—which was once called macrophage activating factor—stimulates macrophages to produce [[nitric oxide]]. The source of interferon-gamma can be [[CD4+ T cells|CD4<sup>+</sup> T cells]], [[CD8+ T cells|CD8<sup>+</sup> T cells]], [[NK cell|natural killer cells]], [[B cells]], [[NKT cell|natural killer T cells]], monocytes, macrophages, or dendritic cells.<ref name="pmid14525967">{{cite journal | author = Schroder K, Hertzog PJ, Ravasi T, Hume DA | title = Interferon-gamma: an overview of signals, mechanisms and functions | journal = J. Leukoc. Biol. | volume = 75 | issue = 2 | pages = 163–89 | date = February 2004 | pmid = 14525967 | doi = 10.1189/jlb.0603252 | last2 = Hertzog | last3 = Ravasi | last4 = Hume | s2cid = 15862242 | doi-access = free }}</ref> Nitric oxide is then released from the macrophage and, because of its toxicity, kills microbes near the macrophage.<ref name=USC/> Activated macrophages produce and secrete [[tumor necrosis factors|tumor necrosis factor]]. This [[cytokine]]—a class of signaling molecule<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=188}}</ref>—kills cancer cells and cells infected by viruses, and helps to activate the other cells of the immune system.<ref name=autogenerated2>{{Harvnb|Sompayrac|2019|p=136}}</ref>
In some diseases, e.g., the rare [[chronic granulomatous disease]], the efficiency of phagocytes is impaired, and recurrent bacterial infections are a problem.<ref name="pmid18846805">{{cite journal
| author = Lipu HN, Ahmed TA, Ali S, Ahmed D, Waqar MA| title = Chronic granulomatous disease| journal = J Pak Med Assoc| volume = 58| issue = 9| pages = 516–18|date=September 2008| pmid = 18846805
| last2 = Ahmed| last3 = Ali| last4 = Ahmed| last5 = Waqar}}</ref> In this disease there is an abnormality affecting different elements of oxygen-dependent killing. Other rare congenital abnormalities, such as [[Chédiak–Higashi syndrome]], are also associated with defective killing of ingested microbes.<ref name="pmid18043242">{{cite journal | author = Kaplan J, De Domenico I, Ward DM | title = Chediak-Higashi syndrome | journal = Curr. Opin. Hematol. | volume = 15 | issue = 1 | pages = 22–29 |date=January 2008 | pmid = 18043242 | doi = 10.1097/MOH.0b013e3282f2bcce | last2 = De Domenico | last3 = Ward | s2cid = 43243529 }}</ref>
=== Viruses ===
[[Virus]]es can reproduce only inside cells, and they gain entry by using many of the receptors involved in immunity. Once inside the cell, viruses use the cell's biological machinery to their own advantage, forcing the cell to make hundreds of identical copies of themselves. Although phagocytes and other components of the innate immune system can, to a limited extent, control viruses, once a virus is inside a cell the adaptive immune responses, particularly the lymphocytes, are more important for defense.<ref>{{Harvnb|Sompayrac|2019|p=7}}</ref> At the sites of viral infections, lymphocytes often vastly outnumber all the other cells of the immune system; this is common in viral [[meningitis]].<ref name="pmid17962876">{{cite journal | author = de Almeida SM, Nogueira MB, Raboni SM, Vidal LR | title = Laboratorial diagnosis of lymphocytic meningitis | journal = Braz J Infect Dis | volume = 11 | issue = 5 | pages = 489–95 |date=October 2007 | pmid = 17962876 | doi = 10.1590/s1413-86702007000500010| last2 = Nogueira | last3 = Raboni | last4 = Vidal | doi-access = free }}</ref> Virus-infected cells that have been killed by lymphocytes are cleared from the body by phagocytes.<ref>{{Harvnb|Sompayrac|2019|p=22}}</ref>
== Role in apoptosis ==
{{main|Apoptosis}}
[[File:Apoptosis.png|thumb|upright|Apoptosis—phagocytes clear fragments of dead cells from the body]]
In an animal, cells are constantly dying. A balance between [[cell division]] and cell death keeps the number of cells relatively constant in adults.<ref name="pathogenesis">{{cite journal | author=Thompson, CB| title=Apoptosis in the pathogenesis and treatment of disease| journal=Science| year=1995| volume=267| issue=5203| pages=1456–62| doi=10.1126/science.7878464| pmid=7878464 | bibcode=1995Sci...267.1456T| s2cid=12991980}}</ref> There are two different ways a cell can die: by [[necrosis]] or by apoptosis. In contrast to necrosis, which often results from disease or trauma, apoptosis—or [[programmed cell death]]—is a normal healthy function of cells. The body has to rid itself of millions of dead or dying cells every day, and phagocytes play a crucial role in this process.<ref>{{Harvnb|Sompayrac|2019|p=68}}</ref>
Dying cells that undergo the final stages of [[apoptosis]]<ref>{{cite web|url=http://www.merriam-webster.com/dictionary/apoptosis |title=Apoptosis |work=Merriam-Webster Online Dictionary |access-date=December 19, 2014 }}</ref> display molecules, such as [[phosphatidylserine]], on their cell surface to attract phagocytes.<ref name="pmid14645847">{{cite journal
| author = Li MO, Sarkisian MR, Mehal WZ, Rakic P, Flavell RA
| title = Phosphatidylserine receptor is required for clearance of apoptotic cells
| journal = Science | volume = 302 | issue = 5650 | pages = 1560–63 |date=November 2003 | pmid = 14645847 | doi = 10.1126/science.1087621 | last2 = Sarkisian
| last3 = Mehal
| last4 = Rakic
| last5 = Flavell
| s2cid = 36252352
| url = https://semanticscholar.org/paper/0946eda3ac2cb65b78a7af7b879f97db91c7023a
}} (Free registration required for online access)</ref> Phosphatidylserine is normally found on the [[cytoplasm|cytosolic]] surface of the plasma membrane, but is redistributed during apoptosis to the extracellular surface by a protein known as [[scramblase]].<ref name="pmid31837595">{{cite journal |vauthors=Nagata S, Sakuragi T, Segawa K |title=Flippase and scramblase for phosphatidylserine exposure |journal=Current Opinion in Immunology |volume=62 |pages=31–38 |date=December 2019 |pmid=31837595 |doi=10.1016/j.coi.2019.11.009 |doi-access=free }}</ref><ref name="phago2">{{cite journal| author=Wang X| title=Cell corpse engulfment mediated by ''C. elegans'' phosphatidylserine receptor through CED-5 and CED-12| journal=Science| year=2003| volume=302| issue=5650| pages=1563–1566| doi=10.1126/science.1087641| pmid=14645848 | bibcode=2003Sci...302.1563W| s2cid=25672278| url=https://semanticscholar.org/paper/ca6fd5581faa5fa9ee33ab1a2d993a910188788c}} (Free registration required for online access)</ref> These molecules mark the cell for phagocytosis by cells that possess the appropriate receptors, such as macrophages.<ref name="phago1">{{cite journal|vauthors=Savill J, Gregory C, Haslett C | title=Eat me or die| journal=Science| year=2003| volume=302| issue=5650| pages=1516–17| doi=10.1126/science.1092533| pmid=14645835| hdl=1842/448| s2cid=13402617| url=https://semanticscholar.org/paper/da2238a1c09adaca71a04c8c04305a189db6c865| hdl-access=free}}</ref> The removal of dying cells by phagocytes occurs in an orderly manner without eliciting an [[inflammatory response]] and is an important function of phagocytes.<ref name="pmid18774293">{{cite journal
| author = Zhou Z, Yu X
| title = Phagosome maturation during the removal of apoptotic cells: receptors lead the way
| journal = Trends Cell Biol. | volume = 18 | issue = 10 | pages = 474–85 |date=October 2008 | pmid = 18774293 | doi = 10.1016/j.tcb.2008.08.002
| pmc = 3125982 | last2 = Yu
}}</ref>
== Interactions with other cells ==
Phagocytes are usually not bound to any particular [[organ (anatomy)|organ]] but move through the body interacting with the other phagocytic and non-phagocytic cells of the immune system. They can communicate with other cells by producing chemicals called [[cytokines]], which recruit other phagocytes to the site of infections or stimulate dormant [[lymphocyte]]s.<ref>{{Harvnb|Sompayrac|2019|p=3}}</ref> Phagocytes form part of the [[innate immune system]], which animals, including humans, are born with. Innate immunity is very effective but non-specific in that it does not discriminate between different sorts of invaders. On the other hand, the [[adaptive immune system]] of jawed vertebrates—the basis of acquired immunity—is highly specialized and can protect against almost any type of invader.<ref>{{Harvnb|Sompayrac|2019|p=4}}</ref> The adaptive immune system is not dependent on phagocytes but lymphocytes, which produce protective proteins called [[antibody|antibodies]], which tag invaders for destruction and prevent viruses from infecting cells.<ref>{{Harvnb|Sompayrac|2019|pp=27–35}}</ref> Phagocytes, in particular dendritic cells and macrophages, stimulate lymphocytes to produce antibodies by an important process called [[antigen]] presentation.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=171–184}}</ref>
=== Antigen presentation ===
{{main|Antigen presentation}}
[[File:MHC Class I processing.svg|thumb|A schematic diagram of the presentation of foreign peptides by MHC 1 molecules]]
Antigen presentation is a process in which some phagocytes move parts of engulfed materials back to the surface of their cells and "present" them to other cells of the immune system.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=456}}</ref> There are two "professional" antigen-presenting cells: macrophages and dendritic cells.<ref name= paper>{{cite web|url=http://pim.medicine.dal.ca/apc.htm|archive-url=https://web.archive.org/web/20080112211805/http://pim.medicine.dal.ca/apc.htm|archive-date=January 12, 2008|title=Antigen Presenting Cells (APC)|publisher=Dalhousie University|work=Immunology for 1st Year Medical Students|author=Timothy Lee|year=2004|access-date=December 19, 2014}}</ref> After engulfment, foreign proteins (the [[antigen]]s) are broken down into [[peptide]]s inside dendritic cells and macrophages. These peptides are then bound to the cell's [[major histocompatibility complex]] (MHC) glycoproteins, which carry the peptides back to the phagocyte's surface where they can be "presented" to lymphocytes.<ref name=ATP/> Mature macrophages do not travel far from the site of infection, but dendritic cells can reach the body's [[lymph node]]s, where there are millions of lymphocytes.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=161}}</ref> This enhances immunity because the lymphocytes respond to the antigens presented by the dendritic cells just as they would at the site of the original infection.<ref>{{Harvnb|Sompayrac|2019|p=8}}</ref> But dendritic cells can also destroy or pacify lymphocytes if they recognize components of the host body; this is necessary to prevent autoimmune reactions. This process is called tolerance.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=237–242}}</ref>
=== Immunological tolerance ===
{{main|Immunological tolerance}}
Dendritic cells also promote immunological tolerance,<ref name=somethingcool>{{cite journal | author = Lange C, Dürr M, Doster H, Melms A, Bischof F | title = Dendritic cell-regulatory T-cell interactions control self-directed immunity | journal = Immunol. Cell Biol. | volume = 85 | issue = 8 | pages = 575–81 | year = 2007 | pmid = 17592494 | doi = 10.1038/sj.icb.7100088 | last2 = Dürr | last3 = Doster | last4 = Melms | last5 = Bischof | s2cid = 36342899 }}</ref> which stops the body from attacking itself. The first type of tolerance is [[central tolerance]], that occurs in the thymus. [[T cell]]s that bind (via their T cell receptor) to self antigen (presented by dendritic cells on MHC molecules) too strongly are induced to die. The second type of immunological tolerance is [[peripheral tolerance]].
Some self reactive T cells escape the thymus for a number of reasons, mainly due to the lack of expression of some self antigens in the thymus. Another type of T cell; T regulatory cells can down regulate self reactive T cells in the periphery.<ref name=rocky>{{cite web|url=http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php|title=Dendritic Cells and Immune Tolerance|last=Steinman|first=Ralph M.|year=2004|publisher=The Rockefeller University|access-date=December 19, 2014|archive-url=https://web.archive.org/web/20090311032056/http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php|archive-date=March 11, 2009|url-status=dead}}</ref> When immunological tolerance fails, [[autoimmune disease]]s can follow.<ref>{{cite journal|title=Immunological tolerance and autoimmunity|journal=Internal and Emergency Medicine|year=2006|first=S|last=Romagnani|volume=1|issue=3|pages=187–96|pmid=17120464|doi=10.1007/BF02934736|s2cid=27585046}}</ref>
== Professional phagocytes ==
[[File:Myeloid cells.png|thumb|Phagocytes derive from stem cells in the bone marrow|alt=A cartoon showing the relationships between a stem cell and mature white blood cells. Eight different types of white blood cell can derive from the same stem cell.]]
Phagocytes of humans and other jawed vertebrates are divided into "professional" and "non-professional" groups based on the efficiency with which they participate in phagocytosis.<ref name=Ernst186/> The professional phagocytes are the [[monocytes]], [[macrophages]], [[neutrophils]], tissue [[dendritic cell]]s and [[mast cell]]s.<ref name= Rob/> One [[litre]] of human blood contains about six billion phagocytes.<ref name=Hoff-values/>
=== Activation ===
All phagocytes, and especially macrophages, exist in degrees of readiness. Macrophages are usually relatively dormant in the tissues and proliferate slowly. In this semi-resting state, they clear away dead host cells and other non-infectious debris and rarely take part in antigen presentation. But, during an infection, they receive chemical signals—usually [[interferon gamma]]—which increases their production of [[MHC class II|MHC II]] molecules and which prepares them for presenting antigens. In this state, macrophages are good antigen presenters and killers. If they receive a signal directly from an invader, they become "hyperactivated", stop proliferating, and concentrate on killing. Their size and rate of phagocytosis increases—some become large enough to engulf invading [[protozoa]].<ref>{{Harvnb|Sompayrac|2019|pp=16–17}}</ref>
In the blood, neutrophils are inactive but are swept along at high speed. When they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill.<ref>{{Harvnb|Sompayrac|2019|pp=18–19}}</ref>
=== Migration ===
[[File:NeutrophilerAktion.svg|thumb|upright|Neutrophils move from the blood to the site of infection|alt=A cartoon depicting a blood vessel and its surrounding tissue cells. There are three similar white blood cells, one in the blood and two among the tissue cells. The ones in the tissue are producing granules that can destroy bacteria.]]
When an infection occurs, a chemical "SOS" signal is given off to attract phagocytes to the site.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=6}}</ref> These chemical signals may include proteins from invading bacteria, clotting system [[peptides]], [[Complement system|complement]] products, and cytokines that have been given off by macrophages located in the tissue near the infection site.<ref name=USC/> Another group of chemical attractants are [[cytokines]] that recruit neutrophils and monocytes from the blood.<ref name=money>Janeway, Chapter: [https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=migration&rid=imm.section.203#206 Induced innate responses to infection.]</ref>
To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the [[endothelial]] cells that line the blood vessels to make a protein called [[selectin]], which neutrophils stick to on passing by. Other signals called [[vasodilator]]s loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. [[Chemotaxis]] is the process by which phagocytes follow the cytokine "scent" to the infected spot.<ref name=USC/> Neutrophils travel across [[epithelial]] cell-lined organs to sites of infection, and although this is an important component of fighting infection, the migration itself can result in disease-like symptoms.<ref name="pmid14519390">{{cite journal | author = Zen K, Parkos CA | title = Leukocyte-epithelial interactions | journal = Curr. Opin. Cell Biol. | volume = 15 | issue = 5 | pages = 557–64 |date=October 2003 | pmid = 14519390 | doi = 10.1016/S0955-0674(03)00103-0| last2 = Parkos}}</ref> During an infection, millions of neutrophils are recruited from the blood, but they die after a few days.<ref>{{Harvnb|Sompayrac|2019|p=18}}</ref>
=== Monocytes ===
{{main|Monocytes}}
[[File:Monocytes, a type of white blood cell (Giemsa stained).jpg|thumb|Monocytes in blood ([[Giemsa stain]])]]
Monocytes develop in the bone marrow and reach maturity in the blood. Mature monocytes have large, smooth, lobed nuclei and abundant [[cytoplasm]] that contains granules. Monocytes ingest foreign or dangerous substances and present [[antigens]] to other cells of the immune system. Monocytes form two groups: a circulating group and a marginal group that remain in other tissues (approximately 70% are in the marginal group). Most monocytes leave the blood stream after 20–40 hours to travel to tissues and organs and in doing so transform into macrophages<ref>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=117}}</ref> or dendritic cells depending on the signals they receive.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=1–6}}</ref> There are about 500 million monocytes in one litre of human blood.<ref name=Hoff-values />
=== Macrophages ===
{{main|Macrophages}}
Mature macrophages do not travel far but stand guard over those areas of the body that are exposed to the outside world. There they act as garbage collectors, antigen presenting cells, or ferocious killers, depending on the signals they receive.<ref>{{Harvnb|Sompayrac|2019|p=136}}</ref> They derive from monocytes, [[granulocyte]] stem cells, or the [[cell division]] of pre-existing macrophages.<ref name="pmid8870002">{{cite journal
| author = Takahashi K, Naito M, Takeya M
| title = Development and heterogeneity of macrophages and their related cells through their differentiation pathways
| journal = Pathol. Int. | volume = 46 | issue = 7 | pages = 473–85 |date=July 1996 | pmid = 8870002 | doi = 10.1111/j.1440-1827.1996.tb03641.x
| last2 = Naito
| last3 = Takeya
| s2cid = 6049656
}}</ref> Human macrophages are about 21 [[micrometre|micrometer]]s in diameter.<ref>{{cite journal |author=Krombach F, Münzing S, Allmeling AM, Gerlach JT, Behr J, Dörger M |title=Cell size of alveolar macrophages: an interspecies comparison |journal=Environ. Health Perspect. |volume=105 Suppl 5 |pages=1261–63 |date=September 1997 |pmid=9400735 |pmc=1470168 |doi= 10.2307/3433544 |jstor=3433544 |issue=Suppl 5|last2=Münzing |last3=Allmeling |last4=Gerlach |last5=Behr |last6=Dörger }}</ref>
[[File:Cutaneous abscess MRSA staphylococcus aureus 7826 lores.jpg|thumb|left|[[Pus]] oozing from an [[abscess]] caused by bacteria—pus contains millions of phagocytes|alt=A person's thigh with a red area that is inflamed. At the centre of the inflammation is a wound with pus.]]
This type of phagocyte does not have granules but contains many [[lysosome]]s. Macrophages are found throughout the body in almost all tissues and organs (e.g., [[microglial cell]]s in the [[brain]] and [[pulmonary alveolus|alveolar]] macrophages in the [[lungs]]), where they silently lie in wait. A macrophage's location can determine its size and appearance. Macrophages cause inflammation through the production of [[interleukin-1]], [[interleukin-6]], and [[Tumor necrosis factor-alpha|TNF-alpha]].<ref name=USCmac>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=31–36}}</ref> Macrophages are usually only found in tissue and are rarely seen in blood circulation. The life-span of tissue macrophages has been estimated to range from four to fifteen days.<ref>{{Harvnb|Ernst|Stendahl|2006|p=8}}</ref>
Macrophages can be activated to perform functions that a resting monocyte cannot.<ref name=USCmac/> [[T helper cell]]s (also known as effector T cells or T<sub>h</sub> cells), a sub-group of lymphocytes, are responsible for the activation of macrophages. T<sub>h</sub>1 cells activate macrophages by signaling with [[IFN-gamma]] and displaying the protein [[CD40 ligand]].<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=156}}</ref> Other signals include TNF-alpha and [[lipopolysaccharides]] from bacteria.<ref name=USCmac/> T<sub>h</sub>1 cells can recruit other phagocytes to the site of the infection in several ways. They secrete cytokines that act on the [[bone marrow]] to stimulate the production of monocytes and neutrophils, and they secrete some of the [[cytokine]]s that are responsible for the migration of monocytes and neutrophils out of the bloodstream.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=187}}</ref> T<sub>h</sub>1 cells come from the [[cellular differentiation|differentiation]] of CD4<sup>+</sup> T cells once they have responded to antigen in the [[lymphatic system|secondary lymphoid tissues]].<ref name=USCmac/> Activated macrophages play a potent role in [[tumor]] destruction by producing TNF-alpha, IFN-gamma, nitric oxide, reactive oxygen compounds, [[cation]]ic proteins, and hydrolytic enzymes.<ref name=USCmac/>
=== Neutrophils ===
{{main|Neutrophils}}
[[File:Neutrophils.jpg|thumb|Neutrophils with a segmented nuclei surrounded by [[erythrocytes]], the intra-cellular granules are visible in the [[cytoplasm]] ([[Giemsa stain]]ed) |alt=A round cell with a lobed nucleus surrounded by many slightly smaller red blood cells.]]
Neutrophils are normally found in the [[circulatory system|bloodstream]] and are the most abundant type of phagocyte, constituting 50% to 60% of the total circulating white blood cells.<ref name="IandF">{{cite book | last = Stvrtinová | first = Viera | author2 = Ján Jakubovský and Ivan Hulín | title = Inflammation and Fever from Pathophysiology: Principles of Disease | publisher = Academic Electronic Press | year = 1995 | location = Computing Centre, Slovak Academy of Sciences | chapter-url = http://nic.sav.sk/logos/books/scientific/node15.html | isbn = 978-80-967366-1-4 | chapter = Neutrophils, central cells in acute inflammation | access-date = December 19, 2014 | url-status = dead | archive-url = https://web.archive.org/web/20101231014453/http://nic.sav.sk/logos/books/scientific/node15.html | archive-date = December 31, 2010 }}</ref> One litre of human blood contains about five billion neutrophils,<ref name=Hoff-values /> which are about 10 micrometers in diameter<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=4}}</ref> and live for only about five days.<ref name=autogenerated2 /> Once they have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection.<ref name=Som18>{{Harvnb|Sompayrac|2019|p=18}}</ref> They are ferocious eaters and rapidly engulf invaders coated with [[antibody|antibodies]] and [[complement system|complement]], and damaged cells or cellular debris. Neutrophils do not return to the blood; they turn into [[pus]] cells and die.<ref name=Som18/> Mature neutrophils are smaller than monocytes and have a segmented [[Cell nucleus|nucleus]] with several sections; each section is connected by [[chromatin]] filaments—neutrophils can have 2–5 segments. Neutrophils do not normally exit the bone marrow until maturity but during an infection neutrophil precursors called [[metamyelocyte]]s, [[myelocyte]]s and [[promyelocyte]]s are released.<ref name="pmid9853933">{{cite journal | author = Linderkamp O, Ruef P, Brenner B, Gulbins E, Lang F | title = Passive deformability of mature, immature, and active neutrophils in healthy and septicemic neonates | journal = Pediatr. Res. | volume = 44 | issue = 6 | pages = 946–50 |date=December 1998 | pmid = 9853933 | doi = 10.1203/00006450-199812000-00021| last2 = Ruef | last3 = Brenner | last4 = Gulbins | last5 = Lang | doi-access = free }}</ref>
The intra-cellular granules of the human neutrophil have long been recognized for their protein-destroying and bactericidal properties.<ref>{{Harvnb|Paoletti|Notario|Ricevuti|1997|p=62}}</ref> Neutrophils can secrete products that stimulate monocytes and macrophages. Neutrophil secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing.<ref name="pmid17991288">{{cite journal | author = Soehnlein O, Kenne E, Rotzius P, Eriksson EE, Lindbom L | title = Neutrophil secretion products regulate anti-bacterial activity in monocytes and macrophages | journal = Clin. Exp. Immunol. | volume = 151 | issue = 1 | pages = 139–45 |date=January 2008 | pmid = 17991288 | pmc = 2276935 | doi = 10.1111/j.1365-2249.2007.03532.x | last2 = Kenne | last3 = Rotzius | last4 = Eriksson | last5 = Lindbom }}</ref> Secretions from the [[azurophilic granules|primary granules]] of neutrophils stimulate the phagocytosis of [[IgG]]-antibody-coated bacteria.<ref name="pmid18787642">{{cite journal |vauthors=Soehnlein O, Kai-Larsen Y, Frithiof R | title = Neutrophil primary granule proteins HBP and HNP1-3 boost bacterial phagocytosis by human and murine macrophages | journal = J. Clin. Invest. | volume = 118 | issue = 10 | pages = 3491–502 |date=October 2008 | pmid = 18787642 | pmc = 2532980 | doi = 10.1172/JCI35740 }}</ref> When encountering bacteria, fungi or activated platelets they produce web-like chromatin structures known as [[neutrophil extracellular traps]] (NETs). Composed mainly of DNA, NETs cause death by a process called netosis – after the pathogens are trapped in NETs they are killed by oxidative and non-oxidative mechanisms.<ref name="pmid28990587">{{cite journal |vauthors=Papayannopoulos V |title=Neutrophil extracellular traps in immunity and disease |journal=Nature Reviews. Immunology |volume=18 |issue=2 |pages=134–147 |date=February 2018 |pmid=28990587 |doi=10.1038/nri.2017.105|s2cid=25067858 }}</ref>
=== Dendritic cells ===
{{main|Dendritic cell}}
[[File:Dendritic cell.JPG|thumb|A dendritic cell|alt=One dendritic cell, which is almost the shape of a star. Its edges are ragged.]]
Dendritic cells are specialized antigen-presenting cells that have long outgrowths called dendrites,<ref name=Steinman>{{cite journal|author=Steinman RM, Cohn ZA|title=Identification of a novel cell type in peripheral lymphoid organs of mice. I. Morphology, quantitation, tissue distribution|journal=J. Exp. Med.|volume=137|issue=5|pages=1142–62|year=1973|pmid=4573839|doi=10.1084/jem.137.5.1142|pmc=2139237|last2=Cohn}}</ref> that help to engulf microbes and other invaders.<ref name=rock>{{cite web|url=http://www.rockefeller.edu/labheads/steinman/steinman-lab.php|title=Dendritic Cells|last=Steinman|first=Ralph|publisher=The Rockefeller University|access-date=December 19, 2014}}</ref><ref name=antigen>{{cite journal | author = Guermonprez P, Valladeau J, Zitvogel L, Théry C, Amigorena S | title = Antigen presentation and T cell stimulation by dendritic cells | journal = Annu. Rev. Immunol. | volume = 20 | pages = 621–67 | year = 2002 | pmid = 11861614 | doi = 10.1146/annurev.immunol.20.100301.064828 | last2 = Valladeau | last3 = Zitvogel | last4 = Théry | last5 = Amigorena }}</ref> Dendritic cells are present in the tissues that are in contact with the external environment, mainly the skin, the inner lining of the nose, the lungs, the stomach, and the intestines.<ref>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=134}}</ref> Once activated, they mature and migrate to the lymphoid tissues where they interact with [[T cells]] and [[B cells]] to initiate and orchestrate the adaptive immune response.<ref>{{cite journal|author=Sallusto F, Lanzavecchia A|title=The instructive role of dendritic cells on T-cell responses|journal=Arthritis Res.|volume=4 Suppl 3|pages=S127–32|year=2002|pmid=12110131|doi=10.1186/ar567|pmc=3240143|issue=Suppl 3|last2=Lanzavecchia}}</ref>
Mature dendritic cells activate [[T helper cell]]s and [[cytotoxic T cell]]s.<ref>{{Harvnb|Sompayrac|2019|pp=45–46}}</ref> The activated helper T cells interact with macrophages and B cells to activate them in turn. In addition, dendritic cells can influence the type of immune response produced; when they travel to the lymphoid areas where T cells are held they can activate T cells, which then differentiate into cytotoxic T cells or helper T cells.<ref name="rock"/>
=== Mast cells ===
{{main|Mast cell}}
Mast cells have [[Toll-like receptor]]s and interact with dendritic cells, B cells, and T cells to help mediate adaptive immune functions.<ref name="pmid19672091">{{cite journal |author=Novak N, Bieber T, Peng WM |title=The immunoglobulin E-Toll-like receptor network |journal=International Archives of Allergy and Immunology |volume=151 |issue=1 |pages=1–7 |year=2010 |pmid=19672091 |doi=10.1159/000232565 |url=https://www.karger.com/Article/PDF/000232565|last2=Bieber |last3=Peng |access-date=December 19, 2014 |doi-access=free }}</ref> Mast cells express [[MHC class II]] molecules and can participate in antigen presentation; however, the mast cell's role in antigen presentation is not very well understood.<ref name="pmid18936782">{{cite journal |author=Kalesnikoff J, Galli SJ |title=New developments in mast cell biology |journal=Nature Immunology |volume=9 |issue=11 |pages=1215–23 |date=November 2008 |pmid=18936782 |pmc=2856637 |doi=10.1038/ni.f.216 |last2=Galli }}</ref> Mast cells can consume and kill [[gram-negative bacteria]] (e.g., [[salmonella]]), and process their antigens.<ref name=mast>{{cite journal | author = Malaviya R, Abraham SN | title = Mast cell modulation of immune responses to bacteria | journal = Immunol. Rev. | volume = 179 | pages = 16–24 |date=February 2001 | pmid = 11292019 | doi = 10.1034/j.1600-065X.2001.790102.x| last2 = Abraham| s2cid = 23115222 }}</ref> They specialize in processing the [[fimbria (bacteriology)|fimbrial proteins]] on the surface of bacteria, which are involved in adhesion to tissues.<ref name="pmid8790416">{{cite journal |author=Connell I, Agace W, Klemm P, Schembri M, Mărild S, Svanborg C |title=Type 1 fimbrial expression enhances ''Escherichia coli'' virulence for the urinary tract |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue=18 |pages=9827–32 |date=September 1996 |pmid=8790416 |pmc=38514 |doi= 10.1073/pnas.93.18.9827|last2=Agace |last3=Klemm |last4=Schembri |last5=Mărild |last6=Svanborg |bibcode=1996PNAS...93.9827C |doi-access=free }}</ref><ref name="pmid8568252">{{cite journal | author = Malaviya R, Twesten NJ, Ross EA, Abraham SN, Pfeifer JD | title = Mast cells process bacterial Ags through a phagocytic route for class I MHC presentation to T cells | journal = J. Immunol. | volume = 156 | issue = 4 | pages = 1490–96 |date=February 1996 | pmid = 8568252 | url = http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=8568252 | last2 = Twesten | last3 = Ross | last4 = Abraham | last5 = Pfeifer | access-date = December 19, 2014 }}</ref> In addition to these functions, mast cells produce cytokines that induce an inflammatory response.<ref name="pmid11424870">{{cite journal | author = Taylor ML, Metcalfe DD | title = Mast cells in allergy and host defense | journal = Allergy Asthma Proc | volume = 22 | issue = 3 | pages = 115–19 | year = 2001 | pmid = 11424870 | doi = 10.2500/108854101778148764| last2 = Metcalfe}}</ref> This is a vital part of the destruction of microbes because the cytokines attract more phagocytes to the site of infection.<ref name=mast/><ref name="pmid22577358">{{cite journal |vauthors=Urb M, Sheppard DC |title=The role of mast cells in the defence against pathogens |journal=PLOS Pathogens |volume=8 |issue=4 |pages=e1002619 |year=2012 |pmid=22577358 |pmc=3343118 |doi=10.1371/journal.ppat.1002619 }}</ref>
{| class="wikitable" style="margin:1em auto 1em auto;"
|+ '''Professional Phagocytes'''<ref name=superman>{{Harvnb|Paoletti|Notario|Ricevuti|1997|p=427}}</ref>
! Main location
! Variety of [[phenotype]]s
|-
| Blood
| neutrophils, monocytes
|-
| Bone marrow
| macrophages, monocytes, [[sinusoid (blood vessel)|sinusoidal cells]], [[List of distinct cell types in the adult human body#Epithelial cells lining closed internal body cavities|lining cells]]
|-
| Bone tissue
| [[osteoclast]]s
|-
| Gut and intestinal [[Peyer's patches]]
| macrophages
|-
| [[Connective tissue]]
| [[histiocyte]]s, macrophages, monocytes, dendritic cells
|-
| Liver
| [[Kupffer cell]]s, monocytes
|-
| Lung
| self-replicating macrophages, monocytes, mast cells, dendritic cells
|-
| [[Lymphatic system|Lymphoid tissue]]
| free and fixed macrophages and monocytes, dendritic cells
|-
| Nervous tissue
| [[microglial cell]]s ([[CD4]]<sup>+</sup>)
|-
| [[Spleen]]
| free and fixed macrophages, monocytes, sinusoidal cells
|-
| [[Thymus]]
| free and fixed macrophages and monocytes
|-
| Skin
| resident [[Langerhans cell]]s, other dendritic cells, conventional macrophages, mast cells
|}
== Non-professional phagocytes ==
Dying cells and foreign organisms are consumed by cells other than the "professional" phagocytes.<ref name="pmid18451871">{{cite journal
| author = Birge RB, Ucker DS
| title = Innate apoptotic immunity: the calming touch of death | journal = Cell Death Differ. | volume = 15 | issue = 7 | pages = 1096–1102 |date=July 2008 | pmid = 18451871 | doi = 10.1038/cdd.2008.58
| last2 = Ucker | doi-access = free }}</ref> These cells include [[epithelial cell]]s, [[endothelial cell]]s, [[fibroblast]]s, and mesenchymal cells. They are called non-professional phagocytes, to emphasize that, in contrast to professional phagocytes, phagocytosis is not their principal function.<ref name="pmid11083817">{{cite journal
| author = Couzinet S, Cejas E, Schittny J, Deplazes P, Weber R, Zimmerli S
| title = Phagocytic uptake of ''Encephalitozoon cuniculi'' by nonprofessional phagocytes| journal = Infect. Immun.| volume = 68 | issue = 12 | pages = 6939–45 |date=December 2000 | pmid = 11083817 | pmc = 97802 | doi = 10.1128/IAI.68.12.6939-6945.2000
| last2 = Cejas| last3 = Schittny| last4 = Deplazes| last5 = Weber| last6 = Zimmerli}}</ref> Fibroblasts, for example, which can phagocytose collagen in the process of remolding scars, will also make some attempt to ingest foreign particles.<ref>{{cite journal | pmid = 11112696 | volume=114 | issue=Pt 1 |date=January 2001 | pages=119–129 | author=Segal G, Lee W, Arora PD, McKee M, Downey G, McCulloch CA | title = Involvement of actin filaments and integrins in the binding step in collagen phagocytosis by human fibroblasts | journal = Journal of Cell Science| last2=Lee | last3=Arora | last4=McKee | last5=Downey | last6=McCulloch | doi=10.1242/jcs.114.1.119 }}</ref>
Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up. This is due to their lack of efficient phagocytic receptors, in particular [[opsonin]]s—which are antibodies and complement attached to invaders by the immune system.<ref name= something/> Additionally, most non-professional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis.<ref name="pmid14732160">{{cite journal |author=Rabinovitch M |title=Professional and non-professional phagocytes: an introduction |journal=Trends Cell Biol. |volume=5 |issue=3 |pages=85–87 |date=March 1995 |pmid=14732160 |doi= 10.1016/S0962-8924(00)88955-2}}</ref>
{| class="wikitable" style="margin:1em auto 1em auto;"
|+ '''Non-professional phagocytes'''<ref name=superman />
! Main location
! Variety of phenotypes
|-
| Blood, lymph and lymph nodes
| Lymphocytes
|-
| Blood, lymph and lymph nodes
| [[natural killer cells|NK]] and LGL cells (large granular lymphocytes)
|-
| Blood
| [[Eosinophils]] and [[Basophils]]<ref name="pmid29321780">{{cite journal |vauthors=Lin A, Loré K |title=Granulocytes: New Members of the Antigen-Presenting Cell Family |journal=Frontiers in Immunology |volume=8 |pages=1781 |date=2017 |pmid=29321780 |pmc=5732227 |doi=10.3389/fimmu.2017.01781 |doi-access=free }}</ref>
|-
| Skin
| [[Epithelial cell]]s
|-
| Blood vessels
| [[Endothelial cell]]s
|-
| Connective tissue
| Fibroblasts
|}
== Pathogen evasion and resistance ==
[[File:Staphylococcus aureus, 50,000x, USDA, ARS, EMU.jpg|right|thumb|upright|Cells of ''Staphylococcus aureus'' bacteria: the large, stringy capsules protect the organisms from attack by phagocytes.|alt=Two round bacteria that are close together and are almost completely covered in a string-like substance.]]
A pathogen is only successful in infecting an organism if it can get past its defenses. Pathogenic bacteria and protozoa have developed a variety of methods to resist attacks by phagocytes, and many actually survive and replicate within phagocytic cells.<ref name=chicken>{{cite web|url=http://textbookofbacteriology.net/antiphago.html|title=Mechanisms of Bacterial Pathogenicity: Bacterial Defense Against Phagocytes|last=Todar|first=Kenneth|publisher=2008|access-date=December 19, 2014}}</ref><ref>{{cite journal |author=Alexander J, Satoskar AR, Russell DG |title=Leishmania species: models of intracellular parasitism |journal=J. Cell Sci. |volume=112 |issue= 18|pages=2993–3002 |date=September 1999 |pmid=10462516 |url=http://jcs.biologists.org/cgi/pmidlookup?view=long&pmid=10462516 |last2=Satoskar |last3=Russell |doi=10.1242/jcs.112.18.2993 |access-date=December 19, 2014 }}</ref>
=== Avoiding contact ===
There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the [[inflammatory response]]; without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis.<ref name=chicken/> Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". ''[[Treponema pallidum]]''—the bacterium that causes [[syphilis]]—hides from phagocytes by coating its surface with [[fibronectin]],<ref name="pmid11973157">{{cite journal| author = Celli J, Finlay BB| title = Bacterial avoidance of phagocytosis| journal = Trends Microbiol.| volume = 10| issue = 5| pages = 232–37|date=May 2002| pmid = 11973157| doi = 10.1016/S0966-842X(02)02343-0| last2 = Finlay}}</ref> which is produced naturally by the body and plays a crucial role in [[wound healing]].<ref name="pmid15992798">{{cite journal | author = Valenick LV, Hsia HC, Schwarzbauer JE | title = Fibronectin fragmentation promotes alpha4beta1 integrin-mediated contraction of a fibrin-fibronectin provisional matrix | journal = Experimental Cell Research | volume = 309 | issue = 1 | pages = 48–55 |date=September 2005 | pmid = 15992798 | doi = 10.1016/j.yexcr.2005.05.024 | last2 = Hsia | last3 = Schwarzbauer }}</ref>
=== Avoiding engulfment ===
Bacteria often produce [[bacterial capsule|capsules]] made of proteins or sugars that coat their cells and interfere with phagocytosis.<ref name=chicken/> Some examples are the K5 capsule and O75 [[O antigen]] found on the surface of ''[[Escherichia coli]]'',<ref name="pmid10417134">{{cite journal | author = Burns SM, Hull SI | title = Loss of resistance to ingestion and phagocytic killing by O(-) and K(-) mutants of a uropathogenic ''Escherichia coli'' O75:K5 strain | journal = Infect. Immun. | volume = 67 | issue = 8 | pages = 3757–62 |date=August 1999 | pmid = 10417134 | pmc = 96650 | doi = 10.1128/IAI.67.8.3757-3762.1999| last2 = Hull}}</ref> and the [[exopolysaccharide]] capsules of ''[[Staphylococcus epidermidis]]''.<ref name="pmid15501828">{{cite journal |vauthors=Vuong C, Kocianova S, Voyich JM | title = A crucial role for exopolysaccharide modification in bacterial biofilm formation, immune evasion, and virulence | journal = J. Biol. Chem. | volume = 279 | issue = 52 | pages = 54881–86 |date=December 2004 | pmid = 15501828 | doi = 10.1074/jbc.M411374200 | doi-access = free }}</ref> ''[[Streptococcus pneumoniae]]'' produces several types of capsule that provide different levels of protection,<ref name="pmid19047408">{{cite journal | author = Melin M, Jarva H, Siira L, Meri S, Käyhty H, Väkeväinen M | title = ''Streptococcus pneumoniae'' capsular serotype 19F is more resistant to C3 deposition and less sensitive to opsonophagocytosis than serotype 6B | journal = Infect. Immun. | volume = 77 | issue = 2 | pages = 676–84 |date=February 2009 | pmid = 19047408 | doi = 10.1128/IAI.01186-08 | pmc = 2632042 | last2 = Jarva | last3 = Siira | last4 = Meri | last5 = Käyhty | last6 = Väkeväinen }}</ref> and [[group A streptococci]] produce proteins such as [[M protein (Streptococcus)|M protein]] and [[fimbria (bacteriology)|fimbrial proteins]] to block engulfment. Some proteins hinder opsonin-related ingestion; ''[[Staphylococcus aureus]]'' produces [[Protein A]] to block antibody receptors, which decreases the effectiveness of opsonins.<ref name="pmid16322743">{{cite journal| author = Foster TJ| title = Immune evasion by staphylococci| journal = Nat. Rev. Microbiol.| volume = 3| issue = 12| pages = 948–58|date=December 2005| pmid = 16322743| doi = 10.1038/nrmicro1289| s2cid = 205496221}}</ref> Enteropathogenic species of the genus [[Yersinia]] bind with the use of the virulence factor [[YopH]] to receptors of phagocytes from which they influence the cells capability to exert phagocytosis.<ref name="pmid11890550">{{cite journal |vauthors=Fällman M, Deleuil F, McGee K |title=Resistance to phagocytosis by Yersinia |journal=International Journal of Medical Microbiology |volume=291 |issue=6–7 |pages=501–9 |date=February 2002 |pmid=11890550 |doi= 10.1078/1438-4221-00159}}</ref>
=== Survival inside the phagocyte ===
[[File:Rickettsia rickettsii.jpg|thumb|right|[[Rickettsia]] are small bacteria—here stained red—that grow in the cytoplasm of non-professional phagocytes.|alt=Two round cells with many tiny rod-shaped bacteria inside.]]
Bacteria have developed ways to survive inside phagocytes, where they continue to evade the immune system.<ref name="pmid11708894">{{cite journal
| author = Sansonetti P
| title = Phagocytosis of bacterial pathogens: implications in the host response
| journal = Semin. Immunol. | volume = 13 | issue = 6 | pages = 381–90 |date=December 2001 | pmid = 11708894 | doi = 10.1006/smim.2001.0335
}}</ref> To get safely inside the phagocyte they express proteins called [[invasin]]s. When inside the cell they remain in the cytoplasm and avoid toxic chemicals contained in the phagolysosomes.<ref name="pmid10064587">{{cite journal
| author = Dersch P, Isberg RR| title = A region of the ''Yersinia pseudotuberculosis'' invasin protein enhances integrin-mediated uptake into mammalian cells and promotes self-association| journal = EMBO J.| volume = 18| issue = 5| pages = 1199–1213|date=March 1999| pmid = 10064587| pmc = 1171211| doi = 10.1093/emboj/18.5.1199
| last2 = Isberg}}</ref> Some bacteria prevent the fusion of a phagosome and lysosome, to form the phagolysosome.<ref name=chicken/> Other pathogens, such as ''[[Leishmania]]'', create a highly modified [[vacuole]] inside the phagocyte, which helps them persist and replicate.<ref>{{cite journal |author=Antoine JC, Prina E, Lang T, Courret N |title=The biogenesis and properties of the parasitophorous vacuoles that harbour ''Leishmania'' in murine macrophages |journal=Trends Microbiol. |volume=6 |issue=10 |pages=392–401 |date=October 1998 |pmid=9807783 |doi=10.1016/S0966-842X(98)01324-9 |last2=Prina |last3=Lang |last4=Courret }}</ref> Some bacteria are capable of living inside of the phagolysosome. ''Staphylococcus aureus'', for example, produces the enzymes [[catalase]] and [[superoxide dismutase]], which break down chemicals—such as hydrogen peroxide—produced by phagocytes to kill bacteria.<ref name="pmid18607538">{{cite journal | author = Das D, Saha SS, Bishayi B | title = Intracellular survival of ''Staphylococcus aureus'': correlating production of catalase and superoxide dismutase with levels of inflammatory cytokines | journal = Inflamm. Res. | volume = 57 | issue = 7 | pages = 340–49 |date=July 2008 | pmid = 18607538 | doi = 10.1007/s00011-007-7206-z | last2 = Saha | last3 = Bishayi | s2cid = 22127111 }}</ref> Bacteria may escape from the phagosome before the formation of the phagolysosome: ''[[Listeria monocytogenes]]'' can make a hole in the phagosome wall using enzymes called [[listeriolysin O]] and [[phospholipase C]].<ref name="pmid17517863">{{cite journal| author = Hara H, Kawamura I, Nomura T, Tominaga T, Tsuchiya K, Mitsuyama M| title = Cytolysin-dependent escape of the bacterium from the phagosome is required but not sufficient for induction of the Th1 immune response against Listeria monocytogenes infection: distinct role of Listeriolysin O determined by cytolysin gene replacement| journal = Infect. Immun.| volume = 75| issue = 8| pages = 3791–3801|date=August 2007| pmid = 17517863| pmc = 1951982| doi = 10.1128/IAI.01779-06| last2 = Kawamura| last3 = Nomura| last4 = Tominaga| last5 = Tsuchiya| last6 = Mitsuyama}}</ref>
=== Killing ===
Bacteria have developed several ways of killing phagocytes.<ref name="pmid16322743" /> These include [[cytolysin]]s, which form pores in the phagocyte's cell membranes, [[streptolysins]] and [[leukocidin]]s, which cause neutrophils' granules to rupture and release toxic substances,<ref name="pmid15819624">{{cite journal| author = Datta V, Myskowski SM, Kwinn LA, Chiem DN, Varki N, Kansal RG, Kotb M, Nizet V| title = Mutational analysis of the group A streptococcal operon encoding streptolysin S and its virulence role in invasive infection| journal = Mol. Microbiol.| volume = 56| issue = 3| pages = 681–95|date=May 2005| pmid = 15819624| doi = 10.1111/j.1365-2958.2005.04583.x| last2 = Myskowski| last3 = Kwinn| last4 = Chiem| last5 = Varki| last6 = Kansal| last7 = Kotb| last8 = Nizet| s2cid = 14748436| doi-access = free}}</ref><ref name="pmid16679003">{{cite journal|author=Iwatsuki K, Yamasaki O, Morizane S, Oono T|title=Staphylococcal cutaneous infections: invasion, evasion and aggression|journal=J. Dermatol. Sci.|volume=42|issue=3|pages=203–14|date=June 2006|pmid=16679003|doi=10.1016/j.jdermsci.2006.03.011|last2=Yamasaki|last3=Morizane|last4=Oono}}</ref> and [[exotoxins]] that reduce the supply of a phagocyte's [[Adenosine triphosphate|ATP]], needed for phagocytosis. After a bacterium is ingested, it may kill the phagocyte by releasing toxins that travel through the phagosome or phagolysosome membrane to target other parts of the cell.<ref name=chicken/>
=== Disruption of cell signaling ===
[[File:Leish amast WBC1 DPDx.JPG|right|thumb|''Leishmania tropica'' amastigotes (arrows) in a macrophage from skin|alt=Many small cells of leishmania inside a much larger cell]]
Some survival strategies often involve disrupting cytokines and other methods of [[cell signaling]] to prevent the phagocyte's responding to invasion.<ref name="pmid15639739">{{cite journal | author = Denkers EY, Butcher BA | title = Sabotage and exploitation in macrophages parasitized by intracellular protozoans | journal = Trends Parasitol. | volume = 21 | issue = 1 | pages = 35–41 |date=January 2005 | pmid = 15639739 | doi = 10.1016/j.pt.2004.10.004 | last2 = Butcher}}</ref> The protozoan parasites ''[[Toxoplasma gondii]]'', ''[[Trypanosoma cruzi]]'', and ''[[Leishmania]]'' infect macrophages, and each has a unique way of taming them.<ref name="pmid15639739"/> Some species of ''Leishmania'' alter the infected macrophage's signalling, repress the production of cytokines and microbicidal molecules—nitric oxide and reactive oxygen species—and compromise antigen presentation.<ref name="pmid16281989">{{cite journal| author = Gregory DJ, Olivier M| title = Subversion of host cell signalling by the protozoan parasite ''Leishmania''| journal = Parasitology| volume = 130 Suppl| pages = S27–35| year = 2005| pmid = 16281989| doi = 10.1017/S0031182005008139
| last2 = Olivier
| s2cid = 24696519}}</ref>
== Host damage by phagocytes ==
Macrophages and neutrophils, in particular, play a central role in the inflammatory process by releasing proteins and small-molecule inflammatory mediators that control infection but can damage host tissue. In general, phagocytes aim to destroy pathogens by engulfing them and subjecting them to a battery of toxic chemicals inside a [[phagolysosome]]. If a phagocyte fails to engulf its target, these toxic agents can be released into the environment (an action referred to as "frustrated phagocytosis"). As these agents are also toxic to host cells, they can cause extensive damage to healthy cells and tissues.<ref>Paoletti pp. 426–30</ref>
When neutrophils release their granule contents in the [[kidney]], the contents of the granule (reactive oxygen compounds and proteases) degrade the [[extracellular matrix]] of host cells and can cause damage to [[glomerular]] cells, affecting their ability to filter blood and causing changes in shape. In addition, [[phospholipase]] products (e.g., [[leukotrienes]]) intensify the damage. This release of substances promotes chemotaxis of more neutrophils to the site of infection, and glomerular cells can be damaged further by the adhesion molecules during the migration of neutrophils. The injury done to the glomerular cells can cause [[kidney failure]].<ref name="pmid10430993">{{cite journal| author = Heinzelmann M, Mercer-Jones MA, Passmore JC| title = Neutrophils and renal failure | journal = Am. J. Kidney Dis. | volume = 34 | issue = 2 | pages = 384–99 |date=August 1999 | pmid = 10430993| doi = 10.1016/S0272-6386(99)70375-6| last2 = Mercer-Jones | last3 = Passmore }}</ref>
Neutrophils also play a key role in the development of most forms of [[acute lung injury]].<ref name="pmid11373504">{{cite journal| author = Lee WL, Downey GP| title = Neutrophil activation and acute lung injury| journal = Curr Opin Crit Care | volume = 7 | issue = 1 | pages = 1–7 |date=February 2001 | pmid = 11373504 | doi = 10.1097/00075198-200102000-00001| last2 = Downey| s2cid = 24164360}}</ref> Here, activated neutrophils release the contents of their toxic granules into the lung environment.<ref name="pmid16319683">{{cite journal | author = Moraes TJ, Zurawska JH, Downey GP | title = Neutrophil granule contents in the pathogenesis of lung injury | journal = Curr. Opin. Hematol. | volume = 13 | issue = 1 | pages = 21–27 |date=January 2006 | pmid = 16319683 | doi = 10.1097/01.moh.0000190113.31027.d5 | last2 = Zurawska | last3 = Downey | s2cid = 29374195 }}</ref> Experiments have shown that a reduction in the number of neutrophils lessens the effects of acute lung injury,<ref name="pmid12682440">{{cite journal| author = Abraham E| title = Neutrophils and acute lung injury| journal = Crit. Care Med. | volume = 31 | issue = 4 Suppl | pages = S195–99 |date=April 2003 | pmid = 12682440 | doi =10.1097/01.CCM.0000057843.47705.E8| s2cid = 4004607| url = https://semanticscholar.org/paper/33d1bbeddab0d02bbd37634dab1e745258500732}}</ref> but treatment by inhibiting neutrophils is not clinically realistic, as it would leave the host vulnerable to infection.<ref name="pmid16319683"/> In the [[liver]], damage by neutrophils can contribute to dysfunction and injury in response to the release of [[endotoxin]]s produced by bacteria, [[sepsis]], trauma, [[alcoholic hepatitis]], [[ischemia]], and [[hypovolemic shock]] resulting from acute [[hemorrhage]].<ref name="pmid9704069">{{cite journal |author=Ricevuti G |title=Host tissue damage by phagocytes |journal=Ann. N. Y. Acad. Sci. |volume=832 |issue= 1|pages=426–48 |date=December 1997 |pmid=9704069 |doi= 10.1111/j.1749-6632.1997.tb46269.x|bibcode=1997NYASA.832..426R |s2cid=10318084 }}</ref>
Chemicals released by macrophages can also damage host tissue. [[Tumor necrosis factor-alpha|TNF-α]] is an important chemical that is released by macrophages that causes the blood in small vessels to clot to prevent an infection from spreading.<ref name="pmid17135502">{{cite journal | author = Charley B, Riffault S, Van Reeth K | title = Porcine innate and adaptative immune responses to influenza and coronavirus infections | journal = Ann. N. Y. Acad. Sci. | volume = 1081 | issue = 1| pages = 130–36 |date=October 2006 | pmid = 17135502 | doi = 10.1196/annals.1373.014 | last2 = Riffault | last3 = Van Reeth | pmc = 7168046 | bibcode = 2006NYASA1081..130C | hdl = 1854/LU-369324 | url = https://biblio.ugent.be/publication/369324 | doi-access = free }}</ref> If a bacterial infection spreads to the blood, TNF-α is released into vital organs, which can cause [[vasodilation]] and a decrease in [[blood plasma|plasma]] volume; these in turn can be followed by [[septic shock]]. During septic shock, TNF-α release causes a blockage of the small vessels that supply blood to the vital organs, and the organs may fail. Septic shock can lead to death.<ref name=money/>
== Evolutionary origins ==
Phagocytosis is common and probably appeared early in [[evolution]],<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> evolving first in unicellular eukaryotes.<ref name="pmid18550419"/> [[Amoeba]]e are unicellular [[protists]] that separated from the tree leading to [[metazoa]] shortly after the divergence of plants, and they share many specific functions with mammalian phagocytic cells.<ref name="pmid18550419">{{cite journal | author = Cosson P, Soldati T | title = Eat, kill or die: when amoeba meets bacteria | journal = Curr. Opin. Microbiol. | volume = 11 | issue = 3 | pages = 271–76 |date=June 2008 | pmid = 18550419 | doi = 10.1016/j.mib.2008.05.005 | last2 = Soldati}}</ref> ''[[Dictyostelium discoideum]]'', for example, is an amoeba that lives in the soil and feeds on bacteria. Like animal phagocytes, it engulfs bacteria by phagocytosis mainly through Toll-like receptors, and it has other biological functions in common with macrophages.<ref name="pmid19081545">{{cite book | author = Bozzaro S, Bucci C, Steinert M | title = Phagocytosis and host-pathogen interactions in Dictyostelium with a look at macrophages | journal = Int Rev Cell Mol Biol | volume = 271 | pages = 253–300 | year = 2008 | pmid = 19081545 | doi = 10.1016/S1937-6448(08)01206-9 | series = International Review of Cell and Molecular Biology | isbn = 9780123747280| last2 = Bucci | last3 = Steinert }}</ref> ''Dictyostelium discoideum'' is social; it aggregates when starved to form a migrating [[Dictyostelid|pseudoplasmodium or slug]]. This multicellular organism eventually will produce a [[fruiting body]] with [[spores]] that are resistant to environmental dangers. Before the formation of fruiting bodies, the cells will migrate as a slug-like organism for several days. During this time, exposure to toxins or bacterial pathogens has the potential to compromise survival of the species by limiting spore production. Some of the amoebae engulf bacteria and absorb toxins while circulating within the slug, and these amoebae eventually die. They are genetically identical to the other amoebae in the slug; their self-sacrifice to protect the other amoebae from bacteria is similar to the self-sacrifice of phagocytes seen in the immune system of higher vertebrates. This ancient immune function in social amoebae suggests an evolutionarily conserved cellular foraging mechanism that might have been adapted to defense functions well before the diversification of amoebae into higher forms.<ref name="pmid17673666">{{cite journal
| author = Chen G, Zhuchenko O, Kuspa A
| title = Immune-like phagocyte activity in the social amoeba | journal = Science | volume = 317 | issue = 5838 | pages = 678–81 |date=August 2007 | pmid = 17673666 | doi = 10.1126/science.1143991
| pmc = 3291017 | last2 = Zhuchenko | last3 = Kuspa | bibcode = 2007Sci...317..678C }}</ref> Phagocytes occur throughout the animal kingdom,<ref name=Delves250 /> from marine sponges to insects and lower and higher vertebrates.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=251–252}}</ref><ref name="pmid19063916">{{cite journal | author = Hanington PC, Tam J, Katzenback BA, Hitchen SJ, Barreda DR, Belosevic M | title = Development of macrophages of cyprinid fish | journal = Dev. Comp. Immunol. | volume = 33 | issue = 4 | pages = 411–29 |date=April 2009 | pmid = 19063916 | doi = 10.1016/j.dci.2008.11.004 | last2 = Tam | last3 = Katzenback | last4 = Hitchen | last5 = Barreda | last6 = Belosevic }}</ref> The ability of amoebae to distinguish between self and non-self is a pivotal one, and is the root of the immune system of many species of amoeba.<ref name=amoebaphage/>
== References ==
{{Reflist|30em}}
;Bibliography
{{Refbegin}}
* {{Cite book |last1=Delves |first1=P. J. |last2=Martin |first2=S. J. |last3=Burton |first3=D. R. |last4=Roit |first4=I. M. |title=Roitt's Essential Immunology |edition=11th |year=2006 |publisher=Blackwell Publishing |location=Malden, MA |isbn=978-1-4051-3603-7 }}
* {{Cite book |editor1-last=Ernst |editor1-first=J. D. |editor2-last=Stendahl |editor2-first=O. |title=Phagocytosis of Bacteria and Bacterial Pathogenicity |year=2006 |publisher=Cambridge University Press |location=New York |isbn=978-0-521-84569-4 }} [http://www.cambridge.org/9780521845694 Website]
* {{Cite book |last1=Hoffbrand |first1=A. V. |last2=Pettit |first2=J. E. |last3=Moss |first3=P. A. H. |title=Essential Haematology |edition=4th |year=2005 |publisher=Blackwell Science |location=London |isbn=978-0-632-05153-3 }}
* {{Cite book |editor1-last=Paoletti |editor1-first=R. |editor2-last=Notario |editor2-first=A. |editor3-last=Ricevuti |editor3-first=G. |title=Phagocytes: Biology, Physiology, Pathology, and Pharmacotherapeutics |year=1997 |publisher=The New York Academy of Sciences |location=New York |isbn=978-1-57331-102-1 }}
* {{Cite book |editor1-last=Robinson |editor1-first=J. P. |editor2-last=Babcock |editor2-first=G. F. |title=Phagocyte Function — A guide for research and clinical evaluation |year=1998 |publisher=Wiley–Liss |location=New York |isbn=978-0-471-12364-4 |url-access=registration |url=https://archive.org/details/phagocytefunctio0000unse }}
* {{Cite book |last=Sompayrac |first=L. |title=How the Immune System Works |edition=6th |year=2019 |publisher=Blackwell Publishing |location=Malden, MA |isbn=978-1-119-54212-4}}
{{Refend}}
== External links ==
{{Library resources box
|onlinebooks=yes
|by=no
|lcheading= Phagocytes
|label=Phagocyte
}}
{{Commons category|Phagocytes}}
* {{MeshName|Phagocytes}}
*[https://www.youtube.com/watch?v=JnlULOjUhSQ White blood cell engulfing bacteria]
{{Blood}}
{{Immune system}}
{{featured article}}
[[Category:Phagocytes| ]]
[[Category:Immune system]]
[[Category:Leukocytes]]' |
New page wikitext, after the edit (new_wikitext) | 'hc3r;iwfghnhktbucu6vhiwer,kpohitv6wuiold;o3pk'oweruisd0[5jiiiiiiii#]4[=l Once inside this phagocyte, the bacterium is trapped in a compartment called a [[phagosome]]. Within one minute the phagosome merges with either a [[lysosome]] or a [[Granule (cell biology)|granule]] to form a [[phagolysosome]]. The bacterium is then subjected to an overwhelming array of killing mechanisms<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–7}}</ref> and is dead a few minutes later.<ref name="pmid8301210"/> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> Phagocytes have voracious appetites; scientists have even fed macrophages with [[iron filings]] and then used a small magnet to separate them from other cells.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref>
[[File:Opsonin.png|thumb|left|Macrophages have special receptors that enhance phagocytosis (not to scale)|alt=A cartoon: The macrophage is depicted as a distorted solid circle. On the surface of the circle is a small y-shaped figure that is connected to a solid rectangle that depicts a bacterium.]]
A phagocyte has many types of receptors on its surface that are used to bind material.<ref name=USC/> They include [[opsonin]] receptors, [[scavenger receptor (immunology)|scavenger receptor]]s, and [[Toll-like receptors]]. Opsonin receptors increase the phagocytosis of bacteria that have been coated with [[immunoglobulin G]] (IgG) [[antibodies]] or with [[complement system|complement]]. "Complement" is the name given to a complex series of protein molecules found in the blood that destroy cells or mark them for destruction.<ref>{{Harvnb|Sompayrac|2019|pp=13–16}}</ref> Scavenger receptors bind to a large range of molecules on the surface of bacterial cells, and Toll-like receptors—so called because of their similarity to well-studied receptors in fruit flies that are encoded by the [[Toll (gene)|Toll gene]]—bind to more specific molecules. Binding to Toll-like receptors increases phagocytosis and causes the phagocyte to release a group of hormones that cause [[inflammation]].<ref name=USC/>
== Methods of killing ==
[[File:Phagocytosis2.png|thumb|Simplified diagram of the phagocytosis and destruction of a bacterial cell|alt=A cartoon that depicts the engulfment of a single bacterium, its passage through a cell where it is digested and released as debris.]]
The killing of microbes is a critical function of phagocytes that is performed either within the phagocyte ([[intracellular]] killing) or outside of the phagocyte ([[extracellular]] killing).<ref name="pmid18684880">{{cite journal
| author = Dale DC, Boxer L, Liles WC
| title = The phagocytes: neutrophils and monocytes
| journal = Blood | volume = 112 | issue = 4 | pages = 935–45 |date=August 2008 | pmid = 18684880 | doi = 10.1182/blood-2007-12-077917 | last2 = Boxer
| last3 = Liles
| s2cid = 746699
| doi-access = free }}</ref>
=== Oxygen-dependent intracellular ===
When a phagocyte ingests bacteria (or any material), its oxygen consumption increases. The increase in oxygen consumption, called a [[respiratory burst]], produces reactive oxygen-containing molecules that are anti-microbial.<ref>{{cite journal|title=Respiratory burst in human neutrophils|journal=Journal of Immunological Methods|date=December 17, 1999|first=C|last=Dahlgren|author2=A Karlsson|volume=232|issue=1–2|pages=3–14|pmid=10618505|doi=10.1016/S0022-1759(99)00146-5}}</ref> The oxygen compounds are toxic to both the invader and the cell itself, so they are kept in compartments inside the cell. This method of killing invading microbes by using the reactive oxygen-containing molecules is referred to as oxygen-dependent intracellular killing, of which there are two types.<ref name = pmid15378046/>
The first type is the oxygen-dependent production of a [[superoxide]],<ref name=USC/> which is an oxygen-rich bacteria-killing substance.<ref>{{cite journal|title=NADPH oxidase|journal=The International Journal of Biochemistry & Cell Biology|year=1996|first=KP|last=Shatwell|author2=AW Segal|volume=28|issue=11|pages=1191–95|pmid=9022278|doi=10.1016/S1357-2725(96)00084-2}}</ref> The superoxide is converted to [[hydrogen peroxide]] and [[singlet oxygen]] by an enzyme called [[superoxide dismutase]]. Superoxides also react with the hydrogen peroxide to produce [[hydroxyl radicals]], which assist in killing the invading microbe.<ref name=USC/>
The second type involves the use of the enzyme [[myeloperoxidase]] from neutrophil granules.<ref name="pmid10519157">{{cite journal | author = Klebanoff SJ | title = Myeloperoxidase | journal = Proc. Assoc. Am. Physicians | volume = 111 | issue = 5 | pages = 383–89 | year = 1999 | pmid = 10519157 | doi = 10.1111/paa.1999.111.5.383}}</ref> When granules fuse with a phagosome, myeloperoxidase is released into the phagolysosome, and this enzyme uses hydrogen peroxide and [[chlorine]] to create [[hypochlorite]], a substance used in domestic [[bleach]]. Hypochlorite is extremely toxic to bacteria.<ref name=USC/> Myeloperoxidase contains a [[heme]] pigment, which accounts for the green color of secretions rich in neutrophils, such as [[pus]] and infected [[sputum]].<ref name="pmid15478278">{{cite journal | author = Meyer KC | title = Neutrophils, myeloperoxidase, and bronchiectasis in cystic fibrosis: green is not good | journal = J. Lab. Clin. Med. | volume = 144 | issue = 3 | pages = 124–26 |date=September 2004 | pmid = 15478278 | doi = 10.1016/j.lab.2004.05.014}}</ref>
=== Oxygen-independent intracellular ===
[[File:Gram-stain of gonorrhoea.jpg|thumb|right|Micrograph of [[Gram-stain]]ed [[pus]] showing ''[[Neisseria gonorrhoeae]]'' bacteria inside phagocytes and their relative sizes|alt=Pus under a microscope, there are many white blood cells with lobed nuclei. Inside some of the cells there are hundreds of bacteria that have been engulfed.]]
Phagocytes can also kill microbes by oxygen-independent methods, but these are not as effective as the oxygen-dependent ones. There are four main types. The first uses electrically charged proteins that damage the bacterium's [[cell membrane|membrane]]. The second type uses lysozymes; these enzymes break down the bacterial [[cell wall]]. The third type uses [[lactoferrin]]s, which are present in neutrophil granules and remove essential iron from bacteria.<ref>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=118}}</ref> The fourth type uses [[proteases]] and [[hydrolytic enzymes]]; these enzymes are used to digest the proteins of destroyed bacteria.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–10}}</ref>
=== Extracellular ===
[[Interferon-gamma]]—which was once called macrophage activating factor—stimulates macrophages to produce [[nitric oxide]]. The source of interferon-gamma can be [[CD4+ T cells|CD4<sup>+</sup> T cells]], [[CD8+ T cells|CD8<sup>+</sup> T cells]], [[NK cell|natural killer cells]], [[B cells]], [[NKT cell|natural killer T cells]], monocytes, macrophages, or dendritic cells.<ref name="pmid14525967">{{cite journal | author = Schroder K, Hertzog PJ, Ravasi T, Hume DA | title = Interferon-gamma: an overview of signals, mechanisms and functions | journal = J. Leukoc. Biol. | volume = 75 | issue = 2 | pages = 163–89 | date = February 2004 | pmid = 14525967 | doi = 10.1189/jlb.0603252 | last2 = Hertzog | last3 = Ravasi | last4 = Hume | s2cid = 15862242 | doi-access = free }}</ref> Nitric oxide is then released from the macrophage and, because of its toxicity, kills microbes near the macrophage.<ref name=USC/> Activated macrophages produce and secrete [[tumor necrosis factors|tumor necrosis factor]]. This [[cytokine]]—a class of signaling molecule<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=188}}</ref>—kills cancer cells and cells infected by viruses, and helps to activate the other cells of the immune system.<ref name=autogenerated2>{{Harvnb|Sompayrac|2019|p=136}}</ref>
In some diseases, e.g., the rare [[chronic granulomatous disease]], the efficiency of phagocytes is impaired, and recurrent bacterial infections are a problem.<ref name="pmid18846805">{{cite journal
| author = Lipu HN, Ahmed TA, Ali S, Ahmed D, Waqar MA| title = Chronic granulomatous disease| journal = J Pak Med Assoc| volume = 58| issue = 9| pages = 516–18|date=September 2008| pmid = 18846805
| last2 = Ahmed| last3 = Ali| last4 = Ahmed| last5 = Waqar}}</ref> In this disease there is an abnormality affecting different elements of oxygen-dependent killing. Other rare congenital abnormalities, such as [[Chédiak–Higashi syndrome]], are also associated with defective killing of ingested microbes.<ref name="pmid18043242">{{cite journal | author = Kaplan J, De Domenico I, Ward DM | title = Chediak-Higashi syndrome | journal = Curr. Opin. Hematol. | volume = 15 | issue = 1 | pages = 22–29 |date=January 2008 | pmid = 18043242 | doi = 10.1097/MOH.0b013e3282f2bcce | last2 = De Domenico | last3 = Ward | s2cid = 43243529 }}</ref>
=== Viruses ===
[[Virus]]es can reproduce only inside cells, and they gain entry by using many of the receptors involved in immunity. Once inside the cell, viruses use the cell's biological machinery to their own advantage, forcing the cell to make hundreds of identical copies of themselves. Although phagocytes and other components of the innate immune system can, to a limited extent, control viruses, once a virus is inside a cell the adaptive immune responses, particularly the lymphocytes, are more important for defense.<ref>{{Harvnb|Sompayrac|2019|p=7}}</ref> At the sites of viral infections, lymphocytes often vastly outnumber all the other cells of the immune system; this is common in viral [[meningitis]].<ref name="pmid17962876">{{cite journal | author = de Almeida SM, Nogueira MB, Raboni SM, Vidal LR | title = Laboratorial diagnosis of lymphocytic meningitis | journal = Braz J Infect Dis | volume = 11 | issue = 5 | pages = 489–95 |date=October 2007 | pmid = 17962876 | doi = 10.1590/s1413-86702007000500010| last2 = Nogueira | last3 = Raboni | last4 = Vidal | doi-access = free }}</ref> Virus-infected cells that have been killed by lymphocytes are cleared from the body by phagocytes.<ref>{{Harvnb|Sompayrac|2019|p=22}}</ref>
== Role in apoptosis ==
{{main|Apoptosis}}
[[File:Apoptosis.png|thumb|upright|Apoptosis—phagocytes clear fragments of dead cells from the body]]
In an animal, cells are constantly dying. A balance between [[cell division]] and cell death keeps the number of cells relatively constant in adults.<ref name="pathogenesis">{{cite journal | author=Thompson, CB| title=Apoptosis in the pathogenesis and treatment of disease| journal=Science| year=1995| volume=267| issue=5203| pages=1456–62| doi=10.1126/science.7878464| pmid=7878464 | bibcode=1995Sci...267.1456T| s2cid=12991980}}</ref> There are two different ways a cell can die: by [[necrosis]] or by apoptosis. In contrast to necrosis, which often results from disease or trauma, apoptosis—or [[programmed cell death]]—is a normal healthy function of cells. The body has to rid itself of millions of dead or dying cells every day, and phagocytes play a crucial role in this process.<ref>{{Harvnb|Sompayrac|2019|p=68}}</ref>
Dying cells that undergo the final stages of [[apoptosis]]<ref>{{cite web|url=http://www.merriam-webster.com/dictionary/apoptosis |title=Apoptosis |work=Merriam-Webster Online Dictionary |access-date=December 19, 2014 }}</ref> display molecules, such as [[phosphatidylserine]], on their cell surface to attract phagocytes.<ref name="pmid14645847">{{cite journal
| author = Li MO, Sarkisian MR, Mehal WZ, Rakic P, Flavell RA
| title = Phosphatidylserine receptor is required for clearance of apoptotic cells
| journal = Science | volume = 302 | issue = 5650 | pages = 1560–63 |date=November 2003 | pmid = 14645847 | doi = 10.1126/science.1087621 | last2 = Sarkisian
| last3 = Mehal
| last4 = Rakic
| last5 = Flavell
| s2cid = 36252352
| url = https://semanticscholar.org/paper/0946eda3ac2cb65b78a7af7b879f97db91c7023a
}} (Free registration required for online access)</ref> Phosphatidylserine is normally found on the [[cytoplasm|cytosolic]] surface of the plasma membrane, but is redistributed during apoptosis to the extracellular surface by a protein known as [[scramblase]].<ref name="pmid31837595">{{cite journal |vauthors=Nagata S, Sakuragi T, Segawa K |title=Flippase and scramblase for phosphatidylserine exposure |journal=Current Opinion in Immunology |volume=62 |pages=31–38 |date=December 2019 |pmid=31837595 |doi=10.1016/j.coi.2019.11.009 |doi-access=free }}</ref><ref name="phago2">{{cite journal| author=Wang X| title=Cell corpse engulfment mediated by ''C. elegans'' phosphatidylserine receptor through CED-5 and CED-12| journal=Science| year=2003| volume=302| issue=5650| pages=1563–1566| doi=10.1126/science.1087641| pmid=14645848 | bibcode=2003Sci...302.1563W| s2cid=25672278| url=https://semanticscholar.org/paper/ca6fd5581faa5fa9ee33ab1a2d993a910188788c}} (Free registration required for online access)</ref> These molecules mark the cell for phagocytosis by cells that possess the appropriate receptors, such as macrophages.<ref name="phago1">{{cite journal|vauthors=Savill J, Gregory C, Haslett C | title=Eat me or die| journal=Science| year=2003| volume=302| issue=5650| pages=1516–17| doi=10.1126/science.1092533| pmid=14645835| hdl=1842/448| s2cid=13402617| url=https://semanticscholar.org/paper/da2238a1c09adaca71a04c8c04305a189db6c865| hdl-access=free}}</ref> The removal of dying cells by phagocytes occurs in an orderly manner without eliciting an [[inflammatory response]] and is an important function of phagocytes.<ref name="pmid18774293">{{cite journal
| author = Zhou Z, Yu X
| title = Phagosome maturation during the removal of apoptotic cells: receptors lead the way
| journal = Trends Cell Biol. | volume = 18 | issue = 10 | pages = 474–85 |date=October 2008 | pmid = 18774293 | doi = 10.1016/j.tcb.2008.08.002
| pmc = 3125982 | last2 = Yu
}}</ref>
== Interactions with other cells ==
Phagocytes are usually not bound to any particular [[organ (anatomy)|organ]] but move through the body interacting with the other phagocytic and non-phagocytic cells of the immune system. They can communicate with other cells by producing chemicals called [[cytokines]], which recruit other phagocytes to the site of infections or stimulate dormant [[lymphocyte]]s.<ref>{{Harvnb|Sompayrac|2019|p=3}}</ref> Phagocytes form part of the [[innate immune system]], which animals, including humans, are born with. Innate immunity is very effective but non-specific in that it does not discriminate between different sorts of invaders. On the other hand, the [[adaptive immune system]] of jawed vertebrates—the basis of acquired immunity—is highly specialized and can protect against almost any type of invader.<ref>{{Harvnb|Sompayrac|2019|p=4}}</ref> The adaptive immune system is not dependent on phagocytes but lymphocytes, which produce protective proteins called [[antibody|antibodies]], which tag invaders for destruction and prevent viruses from infecting cells.<ref>{{Harvnb|Sompayrac|2019|pp=27–35}}</ref> Phagocytes, in particular dendritic cells and macrophages, stimulate lymphocytes to produce antibodies by an important process called [[antigen]] presentation.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=171–184}}</ref>
=== Antigen presentation ===
{{main|Antigen presentation}}
[[File:MHC Class I processing.svg|thumb|A schematic diagram of the presentation of foreign peptides by MHC 1 molecules]]
Antigen presentation is a process in which some phagocytes move parts of engulfed materials back to the surface of their cells and "present" them to other cells of the immune system.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=456}}</ref> There are two "professional" antigen-presenting cells: macrophages and dendritic cells.<ref name= paper>{{cite web|url=http://pim.medicine.dal.ca/apc.htm|archive-url=https://web.archive.org/web/20080112211805/http://pim.medicine.dal.ca/apc.htm|archive-date=January 12, 2008|title=Antigen Presenting Cells (APC)|publisher=Dalhousie University|work=Immunology for 1st Year Medical Students|author=Timothy Lee|year=2004|access-date=December 19, 2014}}</ref> After engulfment, foreign proteins (the [[antigen]]s) are broken down into [[peptide]]s inside dendritic cells and macrophages. These peptides are then bound to the cell's [[major histocompatibility complex]] (MHC) glycoproteins, which carry the peptides back to the phagocyte's surface where they can be "presented" to lymphocytes.<ref name=ATP/> Mature macrophages do not travel far from the site of infection, but dendritic cells can reach the body's [[lymph node]]s, where there are millions of lymphocytes.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=161}}</ref> This enhances immunity because the lymphocytes respond to the antigens presented by the dendritic cells just as they would at the site of the original infection.<ref>{{Harvnb|Sompayrac|2019|p=8}}</ref> But dendritic cells can also destroy or pacify lymphocytes if they recognize components of the host body; this is necessary to prevent autoimmune reactions. This process is called tolerance.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=237–242}}</ref>
=== Immunological tolerance ===
{{main|Immunological tolerance}}
Dendritic cells also promote immunological tolerance,<ref name=somethingcool>{{cite journal | author = Lange C, Dürr M, Doster H, Melms A, Bischof F | title = Dendritic cell-regulatory T-cell interactions control self-directed immunity | journal = Immunol. Cell Biol. | volume = 85 | issue = 8 | pages = 575–81 | year = 2007 | pmid = 17592494 | doi = 10.1038/sj.icb.7100088 | last2 = Dürr | last3 = Doster | last4 = Melms | last5 = Bischof | s2cid = 36342899 }}</ref> which stops the body from attacking itself. The first type of tolerance is [[central tolerance]], that occurs in the thymus. [[T cell]]s that bind (via their T cell receptor) to self antigen (presented by dendritic cells on MHC molecules) too strongly are induced to die. The second type of immunological tolerance is [[peripheral tolerance]].
Some self reactive T cells escape the thymus for a number of reasons, mainly due to the lack of expression of some self antigens in the thymus. Another type of T cell; T regulatory cells can down regulate self reactive T cells in the periphery.<ref name=rocky>{{cite web|url=http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php|title=Dendritic Cells and Immune Tolerance|last=Steinman|first=Ralph M.|year=2004|publisher=The Rockefeller University|access-date=December 19, 2014|archive-url=https://web.archive.org/web/20090311032056/http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php|archive-date=March 11, 2009|url-status=dead}}</ref> When immunological tolerance fails, [[autoimmune disease]]s can follow.<ref>{{cite journal|title=Immunological tolerance and autoimmunity|journal=Internal and Emergency Medicine|year=2006|first=S|last=Romagnani|volume=1|issue=3|pages=187–96|pmid=17120464|doi=10.1007/BF02934736|s2cid=27585046}}</ref>
== Professional phagocytes ==
[[File:Myeloid cells.png|thumb|Phagocytes derive from stem cells in the bone marrow|alt=A cartoon showing the relationships between a stem cell and mature white blood cells. Eight different types of white blood cell can derive from the same stem cell.]]
Phagocytes of humans and other jawed vertebrates are divided into "professional" and "non-professional" groups based on the efficiency with which they participate in phagocytosis.<ref name=Ernst186/> The professional phagocytes are the [[monocytes]], [[macrophages]], [[neutrophils]], tissue [[dendritic cell]]s and [[mast cell]]s.<ref name= Rob/> One [[litre]] of human blood contains about six billion phagocytes.<ref name=Hoff-values/>
=== Activation ===
All phagocytes, and especially macrophages, exist in degrees of readiness. Macrophages are usually relatively dormant in the tissues and proliferate slowly. In this semi-resting state, they clear away dead host cells and other non-infectious debris and rarely take part in antigen presentation. But, during an infection, they receive chemical signals—usually [[interferon gamma]]—which increases their production of [[MHC class II|MHC II]] molecules and which prepares them for presenting antigens. In this state, macrophages are good antigen presenters and killers. If they receive a signal directly from an invader, they become "hyperactivated", stop proliferating, and concentrate on killing. Their size and rate of phagocytosis increases—some become large enough to engulf invading [[protozoa]].<ref>{{Harvnb|Sompayrac|2019|pp=16–17}}</ref>
In the blood, neutrophils are inactive but are swept along at high speed. When they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill.<ref>{{Harvnb|Sompayrac|2019|pp=18–19}}</ref>
=== Migration ===
[[File:NeutrophilerAktion.svg|thumb|upright|Neutrophils move from the blood to the site of infection|alt=A cartoon depicting a blood vessel and its surrounding tissue cells. There are three similar white blood cells, one in the blood and two among the tissue cells. The ones in the tissue are producing granules that can destroy bacteria.]]
When an infection occurs, a chemical "SOS" signal is given off to attract phagocytes to the site.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=6}}</ref> These chemical signals may include proteins from invading bacteria, clotting system [[peptides]], [[Complement system|complement]] products, and cytokines that have been given off by macrophages located in the tissue near the infection site.<ref name=USC/> Another group of chemical attractants are [[cytokines]] that recruit neutrophils and monocytes from the blood.<ref name=money>Janeway, Chapter: [https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=migration&rid=imm.section.203#206 Induced innate responses to infection.]</ref>
To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the [[endothelial]] cells that line the blood vessels to make a protein called [[selectin]], which neutrophils stick to on passing by. Other signals called [[vasodilator]]s loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. [[Chemotaxis]] is the process by which phagocytes follow the cytokine "scent" to the infected spot.<ref name=USC/> Neutrophils travel across [[epithelial]] cell-lined organs to sites of infection, and although this is an important component of fighting infection, the migration itself can result in disease-like symptoms.<ref name="pmid14519390">{{cite journal | author = Zen K, Parkos CA | title = Leukocyte-epithelial interactions | journal = Curr. Opin. Cell Biol. | volume = 15 | issue = 5 | pages = 557–64 |date=October 2003 | pmid = 14519390 | doi = 10.1016/S0955-0674(03)00103-0| last2 = Parkos}}</ref> During an infection, millions of neutrophils are recruited from the blood, but they die after a few days.<ref>{{Harvnb|Sompayrac|2019|p=18}}</ref>
=== Monocytes ===
{{main|Monocytes}}
[[File:Monocytes, a type of white blood cell (Giemsa stained).jpg|thumb|Monocytes in blood ([[Giemsa stain]])]]
Monocytes develop in the bone marrow and reach maturity in the blood. Mature monocytes have large, smooth, lobed nuclei and abundant [[cytoplasm]] that contains granules. Monocytes ingest foreign or dangerous substances and present [[antigens]] to other cells of the immune system. Monocytes form two groups: a circulating group and a marginal group that remain in other tissues (approximately 70% are in the marginal group). Most monocytes leave the blood stream after 20–40 hours to travel to tissues and organs and in doing so transform into macrophages<ref>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=117}}</ref> or dendritic cells depending on the signals they receive.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=1–6}}</ref> There are about 500 million monocytes in one litre of human blood.<ref name=Hoff-values />
=== Macrophages ===
{{main|Macrophages}}
Mature macrophages do not travel far but stand guard over those areas of the body that are exposed to the outside world. There they act as garbage collectors, antigen presenting cells, or ferocious killers, depending on the signals they receive.<ref>{{Harvnb|Sompayrac|2019|p=136}}</ref> They derive from monocytes, [[granulocyte]] stem cells, or the [[cell division]] of pre-existing macrophages.<ref name="pmid8870002">{{cite journal
| author = Takahashi K, Naito M, Takeya M
| title = Development and heterogeneity of macrophages and their related cells through their differentiation pathways
| journal = Pathol. Int. | volume = 46 | issue = 7 | pages = 473–85 |date=July 1996 | pmid = 8870002 | doi = 10.1111/j.1440-1827.1996.tb03641.x
| last2 = Naito
| last3 = Takeya
| s2cid = 6049656
}}</ref> Human macrophages are about 21 [[micrometre|micrometer]]s in diameter.<ref>{{cite journal |author=Krombach F, Münzing S, Allmeling AM, Gerlach JT, Behr J, Dörger M |title=Cell size of alveolar macrophages: an interspecies comparison |journal=Environ. Health Perspect. |volume=105 Suppl 5 |pages=1261–63 |date=September 1997 |pmid=9400735 |pmc=1470168 |doi= 10.2307/3433544 |jstor=3433544 |issue=Suppl 5|last2=Münzing |last3=Allmeling |last4=Gerlach |last5=Behr |last6=Dörger }}</ref>
[[File:Cutaneous abscess MRSA staphylococcus aureus 7826 lores.jpg|thumb|left|[[Pus]] oozing from an [[abscess]] caused by bacteria—pus contains millions of phagocytes|alt=A person's thigh with a red area that is inflamed. At the centre of the inflammation is a wound with pus.]]
This type of phagocyte does not have granules but contains many [[lysosome]]s. Macrophages are found throughout the body in almost all tissues and organs (e.g., [[microglial cell]]s in the [[brain]] and [[pulmonary alveolus|alveolar]] macrophages in the [[lungs]]), where they silently lie in wait. A macrophage's location can determine its size and appearance. Macrophages cause inflammation through the production of [[interleukin-1]], [[interleukin-6]], and [[Tumor necrosis factor-alpha|TNF-alpha]].<ref name=USCmac>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=31–36}}</ref> Macrophages are usually only found in tissue and are rarely seen in blood circulation. The life-span of tissue macrophages has been estimated to range from four to fifteen days.<ref>{{Harvnb|Ernst|Stendahl|2006|p=8}}</ref>
Macrophages can be activated to perform functions that a resting monocyte cannot.<ref name=USCmac/> [[T helper cell]]s (also known as effector T cells or T<sub>h</sub> cells), a sub-group of lymphocytes, are responsible for the activation of macrophages. T<sub>h</sub>1 cells activate macrophages by signaling with [[IFN-gamma]] and displaying the protein [[CD40 ligand]].<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=156}}</ref> Other signals include TNF-alpha and [[lipopolysaccharides]] from bacteria.<ref name=USCmac/> T<sub>h</sub>1 cells can recruit other phagocytes to the site of the infection in several ways. They secrete cytokines that act on the [[bone marrow]] to stimulate the production of monocytes and neutrophils, and they secrete some of the [[cytokine]]s that are responsible for the migration of monocytes and neutrophils out of the bloodstream.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=187}}</ref> T<sub>h</sub>1 cells come from the [[cellular differentiation|differentiation]] of CD4<sup>+</sup> T cells once they have responded to antigen in the [[lymphatic system|secondary lymphoid tissues]].<ref name=USCmac/> Activated macrophages play a potent role in [[tumor]] destruction by producing TNF-alpha, IFN-gamma, nitric oxide, reactive oxygen compounds, [[cation]]ic proteins, and hydrolytic enzymes.<ref name=USCmac/>
=== Neutrophils ===
{{main|Neutrophils}}
[[File:Neutrophils.jpg|thumb|Neutrophils with a segmented nuclei surrounded by [[erythrocytes]], the intra-cellular granules are visible in the [[cytoplasm]] ([[Giemsa stain]]ed) |alt=A round cell with a lobed nucleus surrounded by many slightly smaller red blood cells.]]
Neutrophils are normally found in the [[circulatory system|bloodstream]] and are the most abundant type of phagocyte, constituting 50% to 60% of the total circulating white blood cells.<ref name="IandF">{{cite book | last = Stvrtinová | first = Viera | author2 = Ján Jakubovský and Ivan Hulín | title = Inflammation and Fever from Pathophysiology: Principles of Disease | publisher = Academic Electronic Press | year = 1995 | location = Computing Centre, Slovak Academy of Sciences | chapter-url = http://nic.sav.sk/logos/books/scientific/node15.html | isbn = 978-80-967366-1-4 | chapter = Neutrophils, central cells in acute inflammation | access-date = December 19, 2014 | url-status = dead | archive-url = https://web.archive.org/web/20101231014453/http://nic.sav.sk/logos/books/scientific/node15.html | archive-date = December 31, 2010 }}</ref> One litre of human blood contains about five billion neutrophils,<ref name=Hoff-values /> which are about 10 micrometers in diameter<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=4}}</ref> and live for only about five days.<ref name=autogenerated2 /> Once they have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection.<ref name=Som18>{{Harvnb|Sompayrac|2019|p=18}}</ref> They are ferocious eaters and rapidly engulf invaders coated with [[antibody|antibodies]] and [[complement system|complement]], and damaged cells or cellular debris. Neutrophils do not return to the blood; they turn into [[pus]] cells and die.<ref name=Som18/> Mature neutrophils are smaller than monocytes and have a segmented [[Cell nucleus|nucleus]] with several sections; each section is connected by [[chromatin]] filaments—neutrophils can have 2–5 segments. Neutrophils do not normally exit the bone marrow until maturity but during an infection neutrophil precursors called [[metamyelocyte]]s, [[myelocyte]]s and [[promyelocyte]]s are released.<ref name="pmid9853933">{{cite journal | author = Linderkamp O, Ruef P, Brenner B, Gulbins E, Lang F | title = Passive deformability of mature, immature, and active neutrophils in healthy and septicemic neonates | journal = Pediatr. Res. | volume = 44 | issue = 6 | pages = 946–50 |date=December 1998 | pmid = 9853933 | doi = 10.1203/00006450-199812000-00021| last2 = Ruef | last3 = Brenner | last4 = Gulbins | last5 = Lang | doi-access = free }}</ref>
The intra-cellular granules of the human neutrophil have long been recognized for their protein-destroying and bactericidal properties.<ref>{{Harvnb|Paoletti|Notario|Ricevuti|1997|p=62}}</ref> Neutrophils can secrete products that stimulate monocytes and macrophages. Neutrophil secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing.<ref name="pmid17991288">{{cite journal | author = Soehnlein O, Kenne E, Rotzius P, Eriksson EE, Lindbom L | title = Neutrophil secretion products regulate anti-bacterial activity in monocytes and macrophages | journal = Clin. Exp. Immunol. | volume = 151 | issue = 1 | pages = 139–45 |date=January 2008 | pmid = 17991288 | pmc = 2276935 | doi = 10.1111/j.1365-2249.2007.03532.x | last2 = Kenne | last3 = Rotzius | last4 = Eriksson | last5 = Lindbom }}</ref> Secretions from the [[azurophilic granules|primary granules]] of neutrophils stimulate the phagocytosis of [[IgG]]-antibody-coated bacteria.<ref name="pmid18787642">{{cite journal |vauthors=Soehnlein O, Kai-Larsen Y, Frithiof R | title = Neutrophil primary granule proteins HBP and HNP1-3 boost bacterial phagocytosis by human and murine macrophages | journal = J. Clin. Invest. | volume = 118 | issue = 10 | pages = 3491–502 |date=October 2008 | pmid = 18787642 | pmc = 2532980 | doi = 10.1172/JCI35740 }}</ref> When encountering bacteria, fungi or activated platelets they produce web-like chromatin structures known as [[neutrophil extracellular traps]] (NETs). Composed mainly of DNA, NETs cause death by a process called netosis – after the pathogens are trapped in NETs they are killed by oxidative and non-oxidative mechanisms.<ref name="pmid28990587">{{cite journal |vauthors=Papayannopoulos V |title=Neutrophil extracellular traps in immunity and disease |journal=Nature Reviews. Immunology |volume=18 |issue=2 |pages=134–147 |date=February 2018 |pmid=28990587 |doi=10.1038/nri.2017.105|s2cid=25067858 }}</ref>
=== Dendritic cells ===
{{main|Dendritic cell}}
[[File:Dendritic cell.JPG|thumb|A dendritic cell|alt=One dendritic cell, which is almost the shape of a star. Its edges are ragged.]]
Dendritic cells are specialized antigen-presenting cells that have long outgrowths called dendrites,<ref name=Steinman>{{cite journal|author=Steinman RM, Cohn ZA|title=Identification of a novel cell type in peripheral lymphoid organs of mice. I. Morphology, quantitation, tissue distribution|journal=J. Exp. Med.|volume=137|issue=5|pages=1142–62|year=1973|pmid=4573839|doi=10.1084/jem.137.5.1142|pmc=2139237|last2=Cohn}}</ref> that help to engulf microbes and other invaders.<ref name=rock>{{cite web|url=http://www.rockefeller.edu/labheads/steinman/steinman-lab.php|title=Dendritic Cells|last=Steinman|first=Ralph|publisher=The Rockefeller University|access-date=December 19, 2014}}</ref><ref name=antigen>{{cite journal | author = Guermonprez P, Valladeau J, Zitvogel L, Théry C, Amigorena S | title = Antigen presentation and T cell stimulation by dendritic cells | journal = Annu. Rev. Immunol. | volume = 20 | pages = 621–67 | year = 2002 | pmid = 11861614 | doi = 10.1146/annurev.immunol.20.100301.064828 | last2 = Valladeau | last3 = Zitvogel | last4 = Théry | last5 = Amigorena }}</ref> Dendritic cells are present in the tissues that are in contact with the external environment, mainly the skin, the inner lining of the nose, the lungs, the stomach, and the intestines.<ref>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=134}}</ref> Once activated, they mature and migrate to the lymphoid tissues where they interact with [[T cells]] and [[B cells]] to initiate and orchestrate the adaptive immune response.<ref>{{cite journal|author=Sallusto F, Lanzavecchia A|title=The instructive role of dendritic cells on T-cell responses|journal=Arthritis Res.|volume=4 Suppl 3|pages=S127–32|year=2002|pmid=12110131|doi=10.1186/ar567|pmc=3240143|issue=Suppl 3|last2=Lanzavecchia}}</ref>
Mature dendritic cells activate [[T helper cell]]s and [[cytotoxic T cell]]s.<ref>{{Harvnb|Sompayrac|2019|pp=45–46}}</ref> The activated helper T cells interact with macrophages and B cells to activate them in turn. In addition, dendritic cells can influence the type of immune response produced; when they travel to the lymphoid areas where T cells are held they can activate T cells, which then differentiate into cytotoxic T cells or helper T cells.<ref name="rock"/>
=== Mast cells ===
{{main|Mast cell}}
Mast cells have [[Toll-like receptor]]s and interact with dendritic cells, B cells, and T cells to help mediate adaptive immune functions.<ref name="pmid19672091">{{cite journal |author=Novak N, Bieber T, Peng WM |title=The immunoglobulin E-Toll-like receptor network |journal=International Archives of Allergy and Immunology |volume=151 |issue=1 |pages=1–7 |year=2010 |pmid=19672091 |doi=10.1159/000232565 |url=https://www.karger.com/Article/PDF/000232565|last2=Bieber |last3=Peng |access-date=December 19, 2014 |doi-access=free }}</ref> Mast cells express [[MHC class II]] molecules and can participate in antigen presentation; however, the mast cell's role in antigen presentation is not very well understood.<ref name="pmid18936782">{{cite journal |author=Kalesnikoff J, Galli SJ |title=New developments in mast cell biology |journal=Nature Immunology |volume=9 |issue=11 |pages=1215–23 |date=November 2008 |pmid=18936782 |pmc=2856637 |doi=10.1038/ni.f.216 |last2=Galli }}</ref> Mast cells can consume and kill [[gram-negative bacteria]] (e.g., [[salmonella]]), and process their antigens.<ref name=mast>{{cite journal | author = Malaviya R, Abraham SN | title = Mast cell modulation of immune responses to bacteria | journal = Immunol. Rev. | volume = 179 | pages = 16–24 |date=February 2001 | pmid = 11292019 | doi = 10.1034/j.1600-065X.2001.790102.x| last2 = Abraham| s2cid = 23115222 }}</ref> They specialize in processing the [[fimbria (bacteriology)|fimbrial proteins]] on the surface of bacteria, which are involved in adhesion to tissues.<ref name="pmid8790416">{{cite journal |author=Connell I, Agace W, Klemm P, Schembri M, Mărild S, Svanborg C |title=Type 1 fimbrial expression enhances ''Escherichia coli'' virulence for the urinary tract |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue=18 |pages=9827–32 |date=September 1996 |pmid=8790416 |pmc=38514 |doi= 10.1073/pnas.93.18.9827|last2=Agace |last3=Klemm |last4=Schembri |last5=Mărild |last6=Svanborg |bibcode=1996PNAS...93.9827C |doi-access=free }}</ref><ref name="pmid8568252">{{cite journal | author = Malaviya R, Twesten NJ, Ross EA, Abraham SN, Pfeifer JD | title = Mast cells process bacterial Ags through a phagocytic route for class I MHC presentation to T cells | journal = J. Immunol. | volume = 156 | issue = 4 | pages = 1490–96 |date=February 1996 | pmid = 8568252 | url = http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=8568252 | last2 = Twesten | last3 = Ross | last4 = Abraham | last5 = Pfeifer | access-date = December 19, 2014 }}</ref> In addition to these functions, mast cells produce cytokines that induce an inflammatory response.<ref name="pmid11424870">{{cite journal | author = Taylor ML, Metcalfe DD | title = Mast cells in allergy and host defense | journal = Allergy Asthma Proc | volume = 22 | issue = 3 | pages = 115–19 | year = 2001 | pmid = 11424870 | doi = 10.2500/108854101778148764| last2 = Metcalfe}}</ref> This is a vital part of the destruction of microbes because the cytokines attract more phagocytes to the site of infection.<ref name=mast/><ref name="pmid22577358">{{cite journal |vauthors=Urb M, Sheppard DC |title=The role of mast cells in the defence against pathogens |journal=PLOS Pathogens |volume=8 |issue=4 |pages=e1002619 |year=2012 |pmid=22577358 |pmc=3343118 |doi=10.1371/journal.ppat.1002619 }}</ref>
{| class="wikitable" style="margin:1em auto 1em auto;"
|+ '''Professional Phagocytes'''<ref name=superman>{{Harvnb|Paoletti|Notario|Ricevuti|1997|p=427}}</ref>
! Main location
! Variety of [[phenotype]]s
|-
| Blood
| neutrophils, monocytes
|-
| Bone marrow
| macrophages, monocytes, [[sinusoid (blood vessel)|sinusoidal cells]], [[List of distinct cell types in the adult human body#Epithelial cells lining closed internal body cavities|lining cells]]
|-
| Bone tissue
| [[osteoclast]]s
|-
| Gut and intestinal [[Peyer's patches]]
| macrophages
|-
| [[Connective tissue]]
| [[histiocyte]]s, macrophages, monocytes, dendritic cells
|-
| Liver
| [[Kupffer cell]]s, monocytes
|-
| Lung
| self-replicating macrophages, monocytes, mast cells, dendritic cells
|-
| [[Lymphatic system|Lymphoid tissue]]
| free and fixed macrophages and monocytes, dendritic cells
|-
| Nervous tissue
| [[microglial cell]]s ([[CD4]]<sup>+</sup>)
|-
| [[Spleen]]
| free and fixed macrophages, monocytes, sinusoidal cells
|-
| [[Thymus]]
| free and fixed macrophages and monocytes
|-
| Skin
| resident [[Langerhans cell]]s, other dendritic cells, conventional macrophages, mast cells
|}
== Non-professional phagocytes ==
Dying cells and foreign organisms are consumed by cells other than the "professional" phagocytes.<ref name="pmid18451871">{{cite journal
| author = Birge RB, Ucker DS
| title = Innate apoptotic immunity: the calming touch of death | journal = Cell Death Differ. | volume = 15 | issue = 7 | pages = 1096–1102 |date=July 2008 | pmid = 18451871 | doi = 10.1038/cdd.2008.58
| last2 = Ucker | doi-access = free }}</ref> These cells include [[epithelial cell]]s, [[endothelial cell]]s, [[fibroblast]]s, and mesenchymal cells. They are called non-professional phagocytes, to emphasize that, in contrast to professional phagocytes, phagocytosis is not their principal function.<ref name="pmid11083817">{{cite journal
| author = Couzinet S, Cejas E, Schittny J, Deplazes P, Weber R, Zimmerli S
| title = Phagocytic uptake of ''Encephalitozoon cuniculi'' by nonprofessional phagocytes| journal = Infect. Immun.| volume = 68 | issue = 12 | pages = 6939–45 |date=December 2000 | pmid = 11083817 | pmc = 97802 | doi = 10.1128/IAI.68.12.6939-6945.2000
| last2 = Cejas| last3 = Schittny| last4 = Deplazes| last5 = Weber| last6 = Zimmerli}}</ref> Fibroblasts, for example, which can phagocytose collagen in the process of remolding scars, will also make some attempt to ingest foreign particles.<ref>{{cite journal | pmid = 11112696 | volume=114 | issue=Pt 1 |date=January 2001 | pages=119–129 | author=Segal G, Lee W, Arora PD, McKee M, Downey G, McCulloch CA | title = Involvement of actin filaments and integrins in the binding step in collagen phagocytosis by human fibroblasts | journal = Journal of Cell Science| last2=Lee | last3=Arora | last4=McKee | last5=Downey | last6=McCulloch | doi=10.1242/jcs.114.1.119 }}</ref>
Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up. This is due to their lack of efficient phagocytic receptors, in particular [[opsonin]]s—which are antibodies and complement attached to invaders by the immune system.<ref name= something/> Additionally, most non-professional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis.<ref name="pmid14732160">{{cite journal |author=Rabinovitch M |title=Professional and non-professional phagocytes: an introduction |journal=Trends Cell Biol. |volume=5 |issue=3 |pages=85–87 |date=March 1995 |pmid=14732160 |doi= 10.1016/S0962-8924(00)88955-2}}</ref>
{| class="wikitable" style="margin:1em auto 1em auto;"
|+ '''Non-professional phagocytes'''<ref name=superman />
! Main location
! Variety of phenotypes
|-
| Blood, lymph and lymph nodes
| Lymphocytes
|-
| Blood, lymph and lymph nodes
| [[natural killer cells|NK]] and LGL cells (large granular lymphocytes)
|-
| Blood
| [[Eosinophils]] and [[Basophils]]<ref name="pmid29321780">{{cite journal |vauthors=Lin A, Loré K |title=Granulocytes: New Members of the Antigen-Presenting Cell Family |journal=Frontiers in Immunology |volume=8 |pages=1781 |date=2017 |pmid=29321780 |pmc=5732227 |doi=10.3389/fimmu.2017.01781 |doi-access=free }}</ref>
|-
| Skin
| [[Epithelial cell]]s
|-
| Blood vessels
| [[Endothelial cell]]s
|-
| Connective tissue
| Fibroblasts
|}
== Pathogen evasion and resistance ==
[[File:Staphylococcus aureus, 50,000x, USDA, ARS, EMU.jpg|right|thumb|upright|Cells of ''Staphylococcus aureus'' bacteria: the large, stringy capsules protect the organisms from attack by phagocytes.|alt=Two round bacteria that are close together and are almost completely covered in a string-like substance.]]
A pathogen is only successful in infecting an organism if it can get past its defenses. Pathogenic bacteria and protozoa have developed a variety of methods to resist attacks by phagocytes, and many actually survive and replicate within phagocytic cells.<ref name=chicken>{{cite web|url=http://textbookofbacteriology.net/antiphago.html|title=Mechanisms of Bacterial Pathogenicity: Bacterial Defense Against Phagocytes|last=Todar|first=Kenneth|publisher=2008|access-date=December 19, 2014}}</ref><ref>{{cite journal |author=Alexander J, Satoskar AR, Russell DG |title=Leishmania species: models of intracellular parasitism |journal=J. Cell Sci. |volume=112 |issue= 18|pages=2993–3002 |date=September 1999 |pmid=10462516 |url=http://jcs.biologists.org/cgi/pmidlookup?view=long&pmid=10462516 |last2=Satoskar |last3=Russell |doi=10.1242/jcs.112.18.2993 |access-date=December 19, 2014 }}</ref>
=== Avoiding contact ===
There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the [[inflammatory response]]; without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis.<ref name=chicken/> Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". ''[[Treponema pallidum]]''—the bacterium that causes [[syphilis]]—hides from phagocytes by coating its surface with [[fibronectin]],<ref name="pmid11973157">{{cite journal| author = Celli J, Finlay BB| title = Bacterial avoidance of phagocytosis| journal = Trends Microbiol.| volume = 10| issue = 5| pages = 232–37|date=May 2002| pmid = 11973157| doi = 10.1016/S0966-842X(02)02343-0| last2 = Finlay}}</ref> which is produced naturally by the body and plays a crucial role in [[wound healing]].<ref name="pmid15992798">{{cite journal | author = Valenick LV, Hsia HC, Schwarzbauer JE | title = Fibronectin fragmentation promotes alpha4beta1 integrin-mediated contraction of a fibrin-fibronectin provisional matrix | journal = Experimental Cell Research | volume = 309 | issue = 1 | pages = 48–55 |date=September 2005 | pmid = 15992798 | doi = 10.1016/j.yexcr.2005.05.024 | last2 = Hsia | last3 = Schwarzbauer }}</ref>
=== Avoiding engulfment ===
Bacteria often produce [[bacterial capsule|capsules]] made of proteins or sugars that coat their cells and interfere with phagocytosis.<ref name=chicken/> Some examples are the K5 capsule and O75 [[O antigen]] found on the surface of ''[[Escherichia coli]]'',<ref name="pmid10417134">{{cite journal | author = Burns SM, Hull SI | title = Loss of resistance to ingestion and phagocytic killing by O(-) and K(-) mutants of a uropathogenic ''Escherichia coli'' O75:K5 strain | journal = Infect. Immun. | volume = 67 | issue = 8 | pages = 3757–62 |date=August 1999 | pmid = 10417134 | pmc = 96650 | doi = 10.1128/IAI.67.8.3757-3762.1999| last2 = Hull}}</ref> and the [[exopolysaccharide]] capsules of ''[[Staphylococcus epidermidis]]''.<ref name="pmid15501828">{{cite journal |vauthors=Vuong C, Kocianova S, Voyich JM | title = A crucial role for exopolysaccharide modification in bacterial biofilm formation, immune evasion, and virulence | journal = J. Biol. Chem. | volume = 279 | issue = 52 | pages = 54881–86 |date=December 2004 | pmid = 15501828 | doi = 10.1074/jbc.M411374200 | doi-access = free }}</ref> ''[[Streptococcus pneumoniae]]'' produces several types of capsule that provide different levels of protection,<ref name="pmid19047408">{{cite journal | author = Melin M, Jarva H, Siira L, Meri S, Käyhty H, Väkeväinen M | title = ''Streptococcus pneumoniae'' capsular serotype 19F is more resistant to C3 deposition and less sensitive to opsonophagocytosis than serotype 6B | journal = Infect. Immun. | volume = 77 | issue = 2 | pages = 676–84 |date=February 2009 | pmid = 19047408 | doi = 10.1128/IAI.01186-08 | pmc = 2632042 | last2 = Jarva | last3 = Siira | last4 = Meri | last5 = Käyhty | last6 = Väkeväinen }}</ref> and [[group A streptococci]] produce proteins such as [[M protein (Streptococcus)|M protein]] and [[fimbria (bacteriology)|fimbrial proteins]] to block engulfment. Some proteins hinder opsonin-related ingestion; ''[[Staphylococcus aureus]]'' produces [[Protein A]] to block antibody receptors, which decreases the effectiveness of opsonins.<ref name="pmid16322743">{{cite journal| author = Foster TJ| title = Immune evasion by staphylococci| journal = Nat. Rev. Microbiol.| volume = 3| issue = 12| pages = 948–58|date=December 2005| pmid = 16322743| doi = 10.1038/nrmicro1289| s2cid = 205496221}}</ref> Enteropathogenic species of the genus [[Yersinia]] bind with the use of the virulence factor [[YopH]] to receptors of phagocytes from which they influence the cells capability to exert phagocytosis.<ref name="pmid11890550">{{cite journal |vauthors=Fällman M, Deleuil F, McGee K |title=Resistance to phagocytosis by Yersinia |journal=International Journal of Medical Microbiology |volume=291 |issue=6–7 |pages=501–9 |date=February 2002 |pmid=11890550 |doi= 10.1078/1438-4221-00159}}</ref>
=== Survival inside the phagocyte ===
[[File:Rickettsia rickettsii.jpg|thumb|right|[[Rickettsia]] are small bacteria—here stained red—that grow in the cytoplasm of non-professional phagocytes.|alt=Two round cells with many tiny rod-shaped bacteria inside.]]
Bacteria have developed ways to survive inside phagocytes, where they continue to evade the immune system.<ref name="pmid11708894">{{cite journal
| author = Sansonetti P
| title = Phagocytosis of bacterial pathogens: implications in the host response
| journal = Semin. Immunol. | volume = 13 | issue = 6 | pages = 381–90 |date=December 2001 | pmid = 11708894 | doi = 10.1006/smim.2001.0335
}}</ref> To get safely inside the phagocyte they express proteins called [[invasin]]s. When inside the cell they remain in the cytoplasm and avoid toxic chemicals contained in the phagolysosomes.<ref name="pmid10064587">{{cite journal
| author = Dersch P, Isberg RR| title = A region of the ''Yersinia pseudotuberculosis'' invasin protein enhances integrin-mediated uptake into mammalian cells and promotes self-association| journal = EMBO J.| volume = 18| issue = 5| pages = 1199–1213|date=March 1999| pmid = 10064587| pmc = 1171211| doi = 10.1093/emboj/18.5.1199
| last2 = Isberg}}</ref> Some bacteria prevent the fusion of a phagosome and lysosome, to form the phagolysosome.<ref name=chicken/> Other pathogens, such as ''[[Leishmania]]'', create a highly modified [[vacuole]] inside the phagocyte, which helps them persist and replicate.<ref>{{cite journal |author=Antoine JC, Prina E, Lang T, Courret N |title=The biogenesis and properties of the parasitophorous vacuoles that harbour ''Leishmania'' in murine macrophages |journal=Trends Microbiol. |volume=6 |issue=10 |pages=392–401 |date=October 1998 |pmid=9807783 |doi=10.1016/S0966-842X(98)01324-9 |last2=Prina |last3=Lang |last4=Courret }}</ref> Some bacteria are capable of living inside of the phagolysosome. ''Staphylococcus aureus'', for example, produces the enzymes [[catalase]] and [[superoxide dismutase]], which break down chemicals—such as hydrogen peroxide—produced by phagocytes to kill bacteria.<ref name="pmid18607538">{{cite journal | author = Das D, Saha SS, Bishayi B | title = Intracellular survival of ''Staphylococcus aureus'': correlating production of catalase and superoxide dismutase with levels of inflammatory cytokines | journal = Inflamm. Res. | volume = 57 | issue = 7 | pages = 340–49 |date=July 2008 | pmid = 18607538 | doi = 10.1007/s00011-007-7206-z | last2 = Saha | last3 = Bishayi | s2cid = 22127111 }}</ref> Bacteria may escape from the phagosome before the formation of the phagolysosome: ''[[Listeria monocytogenes]]'' can make a hole in the phagosome wall using enzymes called [[listeriolysin O]] and [[phospholipase C]].<ref name="pmid17517863">{{cite journal| author = Hara H, Kawamura I, Nomura T, Tominaga T, Tsuchiya K, Mitsuyama M| title = Cytolysin-dependent escape of the bacterium from the phagosome is required but not sufficient for induction of the Th1 immune response against Listeria monocytogenes infection: distinct role of Listeriolysin O determined by cytolysin gene replacement| journal = Infect. Immun.| volume = 75| issue = 8| pages = 3791–3801|date=August 2007| pmid = 17517863| pmc = 1951982| doi = 10.1128/IAI.01779-06| last2 = Kawamura| last3 = Nomura| last4 = Tominaga| last5 = Tsuchiya| last6 = Mitsuyama}}</ref>
=== Killing ===
Bacteria have developed several ways of killing phagocytes.<ref name="pmid16322743" /> These include [[cytolysin]]s, which form pores in the phagocyte's cell membranes, [[streptolysins]] and [[leukocidin]]s, which cause neutrophils' granules to rupture and release toxic substances,<ref name="pmid15819624">{{cite journal| author = Datta V, Myskowski SM, Kwinn LA, Chiem DN, Varki N, Kansal RG, Kotb M, Nizet V| title = Mutational analysis of the group A streptococcal operon encoding streptolysin S and its virulence role in invasive infection| journal = Mol. Microbiol.| volume = 56| issue = 3| pages = 681–95|date=May 2005| pmid = 15819624| doi = 10.1111/j.1365-2958.2005.04583.x| last2 = Myskowski| last3 = Kwinn| last4 = Chiem| last5 = Varki| last6 = Kansal| last7 = Kotb| last8 = Nizet| s2cid = 14748436| doi-access = free}}</ref><ref name="pmid16679003">{{cite journal|author=Iwatsuki K, Yamasaki O, Morizane S, Oono T|title=Staphylococcal cutaneous infections: invasion, evasion and aggression|journal=J. Dermatol. Sci.|volume=42|issue=3|pages=203–14|date=June 2006|pmid=16679003|doi=10.1016/j.jdermsci.2006.03.011|last2=Yamasaki|last3=Morizane|last4=Oono}}</ref> and [[exotoxins]] that reduce the supply of a phagocyte's [[Adenosine triphosphate|ATP]], needed for phagocytosis. After a bacterium is ingested, it may kill the phagocyte by releasing toxins that travel through the phagosome or phagolysosome membrane to target other parts of the cell.<ref name=chicken/>
=== Disruption of cell signaling ===
[[File:Leish amast WBC1 DPDx.JPG|right|thumb|''Leishmania tropica'' amastigotes (arrows) in a macrophage from skin|alt=Many small cells of leishmania inside a much larger cell]]
Some survival strategies often involve disrupting cytokines and other methods of [[cell signaling]] to prevent the phagocyte's responding to invasion.<ref name="pmid15639739">{{cite journal | author = Denkers EY, Butcher BA | title = Sabotage and exploitation in macrophages parasitized by intracellular protozoans | journal = Trends Parasitol. | volume = 21 | issue = 1 | pages = 35–41 |date=January 2005 | pmid = 15639739 | doi = 10.1016/j.pt.2004.10.004 | last2 = Butcher}}</ref> The protozoan parasites ''[[Toxoplasma gondii]]'', ''[[Trypanosoma cruzi]]'', and ''[[Leishmania]]'' infect macrophages, and each has a unique way of taming them.<ref name="pmid15639739"/> Some species of ''Leishmania'' alter the infected macrophage's signalling, repress the production of cytokines and microbicidal molecules—nitric oxide and reactive oxygen species—and compromise antigen presentation.<ref name="pmid16281989">{{cite journal| author = Gregory DJ, Olivier M| title = Subversion of host cell signalling by the protozoan parasite ''Leishmania''| journal = Parasitology| volume = 130 Suppl| pages = S27–35| year = 2005| pmid = 16281989| doi = 10.1017/S0031182005008139
| last2 = Olivier
| s2cid = 24696519}}</ref>
== Host damage by phagocytes ==
Macrophages and neutrophils, in particular, play a central role in the inflammatory process by releasing proteins and small-molecule inflammatory mediators that control infection but can damage host tissue. In general, phagocytes aim to destroy pathogens by engulfing them and subjecting them to a battery of toxic chemicals inside a [[phagolysosome]]. If a phagocyte fails to engulf its target, these toxic agents can be released into the environment (an action referred to as "frustrated phagocytosis"). As these agents are also toxic to host cells, they can cause extensive damage to healthy cells and tissues.<ref>Paoletti pp. 426–30</ref>
When neutrophils release their granule contents in the [[kidney]], the contents of the granule (reactive oxygen compounds and proteases) degrade the [[extracellular matrix]] of host cells and can cause damage to [[glomerular]] cells, affecting their ability to filter blood and causing changes in shape. In addition, [[phospholipase]] products (e.g., [[leukotrienes]]) intensify the damage. This release of substances promotes chemotaxis of more neutrophils to the site of infection, and glomerular cells can be damaged further by the adhesion molecules during the migration of neutrophils. The injury done to the glomerular cells can cause [[kidney failure]].<ref name="pmid10430993">{{cite journal| author = Heinzelmann M, Mercer-Jones MA, Passmore JC| title = Neutrophils and renal failure | journal = Am. J. Kidney Dis. | volume = 34 | issue = 2 | pages = 384–99 |date=August 1999 | pmid = 10430993| doi = 10.1016/S0272-6386(99)70375-6| last2 = Mercer-Jones | last3 = Passmore }}</ref>
Neutrophils also play a key role in the development of most forms of [[acute lung injury]].<ref name="pmid11373504">{{cite journal| author = Lee WL, Downey GP| title = Neutrophil activation and acute lung injury| journal = Curr Opin Crit Care | volume = 7 | issue = 1 | pages = 1–7 |date=February 2001 | pmid = 11373504 | doi = 10.1097/00075198-200102000-00001| last2 = Downey| s2cid = 24164360}}</ref> Here, activated neutrophils release the contents of their toxic granules into the lung environment.<ref name="pmid16319683">{{cite journal | author = Moraes TJ, Zurawska JH, Downey GP | title = Neutrophil granule contents in the pathogenesis of lung injury | journal = Curr. Opin. Hematol. | volume = 13 | issue = 1 | pages = 21–27 |date=January 2006 | pmid = 16319683 | doi = 10.1097/01.moh.0000190113.31027.d5 | last2 = Zurawska | last3 = Downey | s2cid = 29374195 }}</ref> Experiments have shown that a reduction in the number of neutrophils lessens the effects of acute lung injury,<ref name="pmid12682440">{{cite journal| author = Abraham E| title = Neutrophils and acute lung injury| journal = Crit. Care Med. | volume = 31 | issue = 4 Suppl | pages = S195–99 |date=April 2003 | pmid = 12682440 | doi =10.1097/01.CCM.0000057843.47705.E8| s2cid = 4004607| url = https://semanticscholar.org/paper/33d1bbeddab0d02bbd37634dab1e745258500732}}</ref> but treatment by inhibiting neutrophils is not clinically realistic, as it would leave the host vulnerable to infection.<ref name="pmid16319683"/> In the [[liver]], damage by neutrophils can contribute to dysfunction and injury in response to the release of [[endotoxin]]s produced by bacteria, [[sepsis]], trauma, [[alcoholic hepatitis]], [[ischemia]], and [[hypovolemic shock]] resulting from acute [[hemorrhage]].<ref name="pmid9704069">{{cite journal |author=Ricevuti G |title=Host tissue damage by phagocytes |journal=Ann. N. Y. Acad. Sci. |volume=832 |issue= 1|pages=426–48 |date=December 1997 |pmid=9704069 |doi= 10.1111/j.1749-6632.1997.tb46269.x|bibcode=1997NYASA.832..426R |s2cid=10318084 }}</ref>
Chemicals released by macrophages can also damage host tissue. [[Tumor necrosis factor-alpha|TNF-α]] is an important chemical that is released by macrophages that causes the blood in small vessels to clot to prevent an infection from spreading.<ref name="pmid17135502">{{cite journal | author = Charley B, Riffault S, Van Reeth K | title = Porcine innate and adaptative immune responses to influenza and coronavirus infections | journal = Ann. N. Y. Acad. Sci. | volume = 1081 | issue = 1| pages = 130–36 |date=October 2006 | pmid = 17135502 | doi = 10.1196/annals.1373.014 | last2 = Riffault | last3 = Van Reeth | pmc = 7168046 | bibcode = 2006NYASA1081..130C | hdl = 1854/LU-369324 | url = https://biblio.ugent.be/publication/369324 | doi-access = free }}</ref> If a bacterial infection spreads to the blood, TNF-α is released into vital organs, which can cause [[vasodilation]] and a decrease in [[blood plasma|plasma]] volume; these in turn can be followed by [[septic shock]]. During septic shock, TNF-α release causes a blockage of the small vessels that supply blood to the vital organs, and the organs may fail. Septic shock can lead to death.<ref name=money/>
== Evolutionary origins ==
Phagocytosis is common and probably appeared early in [[evolution]],<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> evolving first in unicellular eukaryotes.<ref name="pmid18550419"/> [[Amoeba]]e are unicellular [[protists]] that separated from the tree leading to [[metazoa]] shortly after the divergence of plants, and they share many specific functions with mammalian phagocytic cells.<ref name="pmid18550419">{{cite journal | author = Cosson P, Soldati T | title = Eat, kill or die: when amoeba meets bacteria | journal = Curr. Opin. Microbiol. | volume = 11 | issue = 3 | pages = 271–76 |date=June 2008 | pmid = 18550419 | doi = 10.1016/j.mib.2008.05.005 | last2 = Soldati}}</ref> ''[[Dictyostelium discoideum]]'', for example, is an amoeba that lives in the soil and feeds on bacteria. Like animal phagocytes, it engulfs bacteria by phagocytosis mainly through Toll-like receptors, and it has other biological functions in common with macrophages.<ref name="pmid19081545">{{cite book | author = Bozzaro S, Bucci C, Steinert M | title = Phagocytosis and host-pathogen interactions in Dictyostelium with a look at macrophages | journal = Int Rev Cell Mol Biol | volume = 271 | pages = 253–300 | year = 2008 | pmid = 19081545 | doi = 10.1016/S1937-6448(08)01206-9 | series = International Review of Cell and Molecular Biology | isbn = 9780123747280| last2 = Bucci | last3 = Steinert }}</ref> ''Dictyostelium discoideum'' is social; it aggregates when starved to form a migrating [[Dictyostelid|pseudoplasmodium or slug]]. This multicellular organism eventually will produce a [[fruiting body]] with [[spores]] that are resistant to environmental dangers. Before the formation of fruiting bodies, the cells will migrate as a slug-like organism for several days. During this time, exposure to toxins or bacterial pathogens has the potential to compromise survival of the species by limiting spore production. Some of the amoebae engulf bacteria and absorb toxins while circulating within the slug, and these amoebae eventually die. They are genetically identical to the other amoebae in the slug; their self-sacrifice to protect the other amoebae from bacteria is similar to the self-sacrifice of phagocytes seen in the immune system of higher vertebrates. This ancient immune function in social amoebae suggests an evolutionarily conserved cellular foraging mechanism that might have been adapted to defense functions well before the diversification of amoebae into higher forms.<ref name="pmid17673666">{{cite journal
| author = Chen G, Zhuchenko O, Kuspa A
| title = Immune-like phagocyte activity in the social amoeba | journal = Science | volume = 317 | issue = 5838 | pages = 678–81 |date=August 2007 | pmid = 17673666 | doi = 10.1126/science.1143991
| pmc = 3291017 | last2 = Zhuchenko | last3 = Kuspa | bibcode = 2007Sci...317..678C }}</ref> Phagocytes occur throughout the animal kingdom,<ref name=Delves250 /> from marine sponges to insects and lower and higher vertebrates.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=251–252}}</ref><ref name="pmid19063916">{{cite journal | author = Hanington PC, Tam J, Katzenback BA, Hitchen SJ, Barreda DR, Belosevic M | title = Development of macrophages of cyprinid fish | journal = Dev. Comp. Immunol. | volume = 33 | issue = 4 | pages = 411–29 |date=April 2009 | pmid = 19063916 | doi = 10.1016/j.dci.2008.11.004 | last2 = Tam | last3 = Katzenback | last4 = Hitchen | last5 = Barreda | last6 = Belosevic }}</ref> The ability of amoebae to distinguish between self and non-self is a pivotal one, and is the root of the immune system of many species of amoeba.<ref name=amoebaphage/>
== References ==
{{Reflist|30em}}
;Bibliography
{{Refbegin}}
* {{Cite book |last1=Delves |first1=P. J. |last2=Martin |first2=S. J. |last3=Burton |first3=D. R. |last4=Roit |first4=I. M. |title=Roitt's Essential Immunology |edition=11th |year=2006 |publisher=Blackwell Publishing |location=Malden, MA |isbn=978-1-4051-3603-7 }}
* {{Cite book |editor1-last=Ernst |editor1-first=J. D. |editor2-last=Stendahl |editor2-first=O. |title=Phagocytosis of Bacteria and Bacterial Pathogenicity |year=2006 |publisher=Cambridge University Press |location=New York |isbn=978-0-521-84569-4 }} [http://www.cambridge.org/9780521845694 Website]
* {{Cite book |last1=Hoffbrand |first1=A. V. |last2=Pettit |first2=J. E. |last3=Moss |first3=P. A. H. |title=Essential Haematology |edition=4th |year=2005 |publisher=Blackwell Science |location=London |isbn=978-0-632-05153-3 }}
* {{Cite book |editor1-last=Paoletti |editor1-first=R. |editor2-last=Notario |editor2-first=A. |editor3-last=Ricevuti |editor3-first=G. |title=Phagocytes: Biology, Physiology, Pathology, and Pharmacotherapeutics |year=1997 |publisher=The New York Academy of Sciences |location=New York |isbn=978-1-57331-102-1 }}
* {{Cite book |editor1-last=Robinson |editor1-first=J. P. |editor2-last=Babcock |editor2-first=G. F. |title=Phagocyte Function — A guide for research and clinical evaluation |year=1998 |publisher=Wiley–Liss |location=New York |isbn=978-0-471-12364-4 |url-access=registration |url=https://archive.org/details/phagocytefunctio0000unse }}
* {{Cite book |last=Sompayrac |first=L. |title=How the Immune System Works |edition=6th |year=2019 |publisher=Blackwell Publishing |location=Malden, MA |isbn=978-1-119-54212-4}}
{{Refend}}
== External links ==
{{Library resources box
|onlinebooks=yes
|by=no
|lcheading= Phagocytes
|label=Phagocyte
}}
{{Commons category|Phagocytes}}
* {{MeshName|Phagocytes}}
*[https://www.youtube.com/watch?v=JnlULOjUhSQ White blood cell engulfing bacteria]
{{Blood}}
{{Immune system}}
{{featured article}}
[[Category:Phagocytes| ]]
[[Category:Immune system]]
[[Category:Leukocytes]]' |
Unified diff of changes made by edit (edit_diff) | '@@ -1,27 +1,3 @@
-{{pp-move-indef}}
-{{short description|Cells that ingest harmful matter within the body}}
-{{Use mdy dates|date=November 2021}}
-[[File:Neutrophil with anthrax copy.jpg|thumb|[[Scanning electron microscope|Scanning electron micrograph]] of a [[Neutrophil granulocyte|neutrophil]] phagocytosing [[Bacillus anthracis|anthrax bacilli]] (orange)|alt= Long rod-shaped bacteria, one of which has been partially engulfed by a larger blob-shaped white blood cell. The shape of the cell is distorted by undigested bacterium inside it.]]
-
-'''Phagocytes''' are [[cell (biology)|cell]]s that protect the body by ingesting harmful foreign particles, [[bacteria]], and dead or [[Apoptosis|dying]] cells. Their name comes from the [[Greek language|Greek]] ''{{lang|grc-Latn|phagein}}'', "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek ''kutos'', "hollow vessel".<ref name=ox>{{cite book|authors=Little, C., Fowler H.W., Coulson J.| title=The Shorter Oxford English Dictionary| publisher=Oxford University Press (Guild Publishing)| year=1983|pages=1566–67}}</ref> They are essential for fighting infections and for subsequent [[immunity (medical)|immunity]].<ref name=USC>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=2–10}}</ref> Phagocytes are important throughout the animal kingdom<ref name=Delves250>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=250}}</ref> and are highly developed within vertebrates.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=251}}</ref> One [[litre]] of human blood contains about six billion phagocytes.<ref name=Hoff-values>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=331}}</ref> They were discovered in 1882 by [[Élie Metchnikoff|Ilya Ilyich Mechnikov]] while he was studying [[starfish]] [[larva]]e.<ref name= Ilya>[http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html Ilya Mechnikov], retrieved on November 28, 2008. From [http://nobelprize.org/nobelfoundation/publications/lectures/index.html Nobel Lectures], ''Physiology or Medicine 1901–1921'', Elsevier Publishing Company, Amsterdam, 1967. {{webarchive |url=https://web.archive.org/web/20080822041214/http://nobelprize.org/nobelfoundation/publications/lectures/index.html |date=August 22, 2008 }}</ref> Mechnikov was awarded the 1908 [[Nobel Prize in Physiology or Medicine]] for his discovery.<ref name=Paul>{{cite journal|title=Ilya Ilich Metchnikoff (1845–1915) and Paul Ehrlich (1854–1915): the centennial of the 1908 Nobel Prize in Physiology or Medicine|journal=Journal of Medical Biography|year=2008|first=FC|last=Schmalstieg|author2=AS Goldman|volume=16|issue=2|pages=96–103|pmid=18463079|doi=10.1258/jmb.2008.008006|s2cid=25063709}}</ref> Phagocytes occur in many species; some [[amoeboid|amoebae]] behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.<ref name=amoebaphage>Janeway, Chapter: [https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=phagocytes,evolution&rid=imm.section.2367#2368 Evolution of the innate immune system.] retrieved on March 20, 2009</ref>
-
-Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at [[phagocytosis]].<ref name=Ernst186>{{Harvnb|Ernst|Stendahl|2006|p=186}}</ref> The professional phagocytes include many types of [[white blood cell]]s (such as [[neutrophil]]s, [[monocyte]]s, [[macrophage]]s, [[mast cell]]s, and [[dendritic cell]]s).<ref name=Rob>{{Harvnb|Robinson|Babcock|1998|p=187}} and {{Harvnb|Ernst|Stendahl|2006|pp=7–10}}</ref> The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called [[receptor (biochemistry)|receptors]] on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body.<ref name= something>{{Harvnb|Ernst|Stendahl|2006|p=10}}</ref> Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan.<ref name="pathogenesis"/>
-
-During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called [[chemotaxis]]. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte.<ref name=money/> Some phagocytes kill the ingested pathogen with [[reactive oxygen species|oxidants]] and [[nitric oxide]].<ref name=pmid15378046>{{cite journal |author=Fang FC |title=Antimicrobial reactive oxygen and nitrogen species: concepts and controversies |journal=Nat. Rev. Microbiol. |volume=2 |issue=10 |pages=820–32 |date=October 2004 |pmid=15378046 |doi=10.1038/nrmicro1004 |s2cid=11063073 }}</ref> After phagocytosis, macrophages and dendritic cells can also participate in [[antigen presentation]], a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's [[lymph node]]s and display the material to white blood cells called [[lymphocytes]]. This process is important in building immunity,<ref name=ATP>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=172–84}}</ref> and many pathogens have evolved methods to evade attacks by phagocytes.<ref name=USC/>
-
-== History ==
-[[File:Professeur Metchnikoff, portrait du scientifique dans un laboratoire de recherche.jpg|thumb|Ilya Ilyich Mechnikov in his laboratory|alt=A bearded old man holding up a test tube. He is sitting at a table by a window. The table is covered with many small bottles and test tubes.]]
-The Russian zoologist [[Ilya Ilyich Mechnikov]] (1845–1916) first recognized that specialized cells were involved in defense against microbial infections.<ref name="pmid31001278">{{cite journal |vauthors=Kaufmann SH|title=Immunology's Coming of Age |journal=Frontiers in Immunology |volume=10 |pages=684 |date=2019 |pmid=31001278 |pmc=6456699 |doi=10.3389/fimmu.2019.00684 |doi-access=free }}</ref> In 1882, he studied [[motility|motile]] (freely moving) cells in the [[larva]]e of [[Sea star|starfishes]], believing they were important to the animals' immune defenses. To test his idea, he inserted small thorns from a [[tangerine]] tree into the larvae. After a few hours he noticed that the motile cells had surrounded the thorns.<ref name="pmid31001278"/> Mechnikov traveled to [[Vienna]] and shared his ideas with [[Carl Friedrich Wilhelm Claus|Carl Friedrich Claus]] who suggested the name "phagocyte" (from the Greek words ''{{lang|grc-Latn|phagein}}'', meaning "to eat or devour", and ''{{lang|grc-Latn|kutos}}'', meaning "hollow vessel"<ref name=ox />) for the cells that Mechnikov had observed.<ref name="pmid9544583">{{cite journal | author = Aterman K | title = Medals, memoirs—and Metchnikoff | journal = J. Leukoc. Biol. | volume = 63 | issue = 4 | pages = 515–17 | date = April 1, 1998 | pmid = 9544583 | doi = 10.1002/jlb.63.4.515 | s2cid = 44748502 | doi-access = free }}</ref>
-
-A year later, Mechnikov studied a fresh water [[crustacean]] called ''[[Daphnia]]'', a tiny transparent animal that can be examined directly under a microscope. He discovered that fungal spores that attacked the animal were destroyed by phagocytes. He went on to extend his observations to the white blood cells of mammals and discovered that the bacterium ''[[Bacillus anthracis]]'' could be engulfed and killed by phagocytes, a process that he called [[phagocytosis]].<ref name=autogenerated5>{{cite web|url=http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html|title=Ilya Mechnikov|publisher=The Nobel Foundation|access-date=December 19, 2014}}</ref> Mechnikov proposed that phagocytes were a primary defense against invading organisms.<ref name="pmid31001278"/>
-
-In 1903, [[Almroth Wright]] discovered that phagocytosis was reinforced by specific [[antibody|antibodies]] that he called [[opsonin]]s, from the Greek ''[[opson]]'', "a dressing or relish".<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=263}}</ref> Mechnikov was awarded (jointly with [[Paul Ehrlich]]) the 1908 [[Nobel Prize in Physiology or Medicine]] for his work on phagocytes and phagocytosis.<ref name= Paul/>
-
-Although the importance of these discoveries slowly gained acceptance during the early twentieth century, the intricate relationships between phagocytes and all the other components of the immune system were not known until the 1980s.<ref>{{Harvnb|Robinson|Babcock|1998|p=vii}}</ref>
-
-== Phagocytosis ==
-{{main|Phagocytosis}}
-[[File:Phagocytosis in three steps.png|thumb|Phagocytosis in three steps: 1. Unbound phagocyte surface receptors do not trigger phagocytosis. 2. Binding of receptors causes them to cluster. 3. Phagocytosis is triggered and the particle is taken up by the phagocyte.|alt=A cartoon: 1. The particle is depicted by an oval and the surface of the phagocyte by a straight line. Different smaller shapes are on the line and the oval. 2. The smaller particles on each surface join. 3. The line is now concave and partially wraps around the oval.]]
-Phagocytosis is the process of taking in particles such as bacteria, invasive [[fungi]], parasites, [[apoptosis|dead host cells]], and cellular and foreign debris by a cell.<ref name=superman2>{{Harvnb|Ernst|Stendahl|2006|p=4}}</ref> It involves a chain of molecular processes.<ref>{{Harvnb|Ernst|Stendahl|2006|p=78}}</ref><ref name="pmid29727727">{{cite journal |vauthors=Feldman MB, Vyas JM, Mansour MK |title=It takes a village: Phagocytes play a central role in fungal immunity |journal=Seminars in Cell & Developmental Biology |volume=89 |issue= |pages=16–23 |date=May 2019 |pmid=29727727 |pmc=6235731 |doi=10.1016/j.semcdb.2018.04.008}}</ref> Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called "receptors" that are on the surface of the phagocyte. The phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes.<ref name="pmid8301210">{{cite journal | author = Hampton MB, Vissers MC, Winterbourn CC | title = A single assay for measuring the rates of phagocytosis and bacterial killing by neutrophils | journal = J. Leukoc. Biol. | volume = 55 | issue = 2 | pages = 147–52 | date = February 1994 | pmid = 8301210 | doi = 10.1002/jlb.55.2.147| url = http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210 | archive-url = https://archive.today/20121228084302/http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210 | url-status = dead | archive-date = December 28, 2012 | last2 = Vissers | last3 = Winterbourn | s2cid = 44911791 | access-date = December 19, 2014 }}</ref> Once inside this phagocyte, the bacterium is trapped in a compartment called a [[phagosome]]. Within one minute the phagosome merges with either a [[lysosome]] or a [[Granule (cell biology)|granule]] to form a [[phagolysosome]]. The bacterium is then subjected to an overwhelming array of killing mechanisms<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–7}}</ref> and is dead a few minutes later.<ref name="pmid8301210"/> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> Phagocytes have voracious appetites; scientists have even fed macrophages with [[iron filings]] and then used a small magnet to separate them from other cells.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref>
+hc3r;iwfghnhktbucu6vhiwer,kpohitv6wuiold;o3pk'oweruisd0[5jiiiiiiii#]4[=l Once inside this phagocyte, the bacterium is trapped in a compartment called a [[phagosome]]. Within one minute the phagosome merges with either a [[lysosome]] or a [[Granule (cell biology)|granule]] to form a [[phagolysosome]]. The bacterium is then subjected to an overwhelming array of killing mechanisms<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–7}}</ref> and is dead a few minutes later.<ref name="pmid8301210"/> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> Phagocytes have voracious appetites; scientists have even fed macrophages with [[iron filings]] and then used a small magnet to separate them from other cells.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref>
[[File:Opsonin.png|thumb|left|Macrophages have special receptors that enhance phagocytosis (not to scale)|alt=A cartoon: The macrophage is depicted as a distorted solid circle. On the surface of the circle is a small y-shaped figure that is connected to a solid rectangle that depicts a bacterium.]]
A phagocyte has many types of receptors on its surface that are used to bind material.<ref name=USC/> They include [[opsonin]] receptors, [[scavenger receptor (immunology)|scavenger receptor]]s, and [[Toll-like receptors]]. Opsonin receptors increase the phagocytosis of bacteria that have been coated with [[immunoglobulin G]] (IgG) [[antibodies]] or with [[complement system|complement]]. "Complement" is the name given to a complex series of protein molecules found in the blood that destroy cells or mark them for destruction.<ref>{{Harvnb|Sompayrac|2019|pp=13–16}}</ref> Scavenger receptors bind to a large range of molecules on the surface of bacterial cells, and Toll-like receptors—so called because of their similarity to well-studied receptors in fruit flies that are encoded by the [[Toll (gene)|Toll gene]]—bind to more specific molecules. Binding to Toll-like receptors increases phagocytosis and causes the phagocyte to release a group of hormones that cause [[inflammation]].<ref name=USC/>
' |
New page size (new_size) | 65928 |
Old page size (old_size) | 76788 |
Size change in edit (edit_delta) | -10860 |
Lines added in edit (added_lines) | [
0 => 'hc3r;iwfghnhktbucu6vhiwer,kpohitv6wuiold;o3pk'oweruisd0[5jiiiiiiii#]4[=l Once inside this phagocyte, the bacterium is trapped in a compartment called a [[phagosome]]. Within one minute the phagosome merges with either a [[lysosome]] or a [[Granule (cell biology)|granule]] to form a [[phagolysosome]]. The bacterium is then subjected to an overwhelming array of killing mechanisms<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–7}}</ref> and is dead a few minutes later.<ref name="pmid8301210"/> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> Phagocytes have voracious appetites; scientists have even fed macrophages with [[iron filings]] and then used a small magnet to separate them from other cells.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref>'
] |
Lines removed in edit (removed_lines) | [
0 => '{{pp-move-indef}}',
1 => '{{short description|Cells that ingest harmful matter within the body}}',
2 => '{{Use mdy dates|date=November 2021}}',
3 => '[[File:Neutrophil with anthrax copy.jpg|thumb|[[Scanning electron microscope|Scanning electron micrograph]] of a [[Neutrophil granulocyte|neutrophil]] phagocytosing [[Bacillus anthracis|anthrax bacilli]] (orange)|alt= Long rod-shaped bacteria, one of which has been partially engulfed by a larger blob-shaped white blood cell. The shape of the cell is distorted by undigested bacterium inside it.]]',
4 => '',
5 => ''''Phagocytes''' are [[cell (biology)|cell]]s that protect the body by ingesting harmful foreign particles, [[bacteria]], and dead or [[Apoptosis|dying]] cells. Their name comes from the [[Greek language|Greek]] ''{{lang|grc-Latn|phagein}}'', "to eat" or "devour", and "-cyte", the suffix in biology denoting "cell", from the Greek ''kutos'', "hollow vessel".<ref name=ox>{{cite book|authors=Little, C., Fowler H.W., Coulson J.| title=The Shorter Oxford English Dictionary| publisher=Oxford University Press (Guild Publishing)| year=1983|pages=1566–67}}</ref> They are essential for fighting infections and for subsequent [[immunity (medical)|immunity]].<ref name=USC>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=2–10}}</ref> Phagocytes are important throughout the animal kingdom<ref name=Delves250>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=250}}</ref> and are highly developed within vertebrates.<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=251}}</ref> One [[litre]] of human blood contains about six billion phagocytes.<ref name=Hoff-values>{{Harvnb|Hoffbrand|Pettit|Moss|2005|p=331}}</ref> They were discovered in 1882 by [[Élie Metchnikoff|Ilya Ilyich Mechnikov]] while he was studying [[starfish]] [[larva]]e.<ref name= Ilya>[http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html Ilya Mechnikov], retrieved on November 28, 2008. From [http://nobelprize.org/nobelfoundation/publications/lectures/index.html Nobel Lectures], ''Physiology or Medicine 1901–1921'', Elsevier Publishing Company, Amsterdam, 1967. {{webarchive |url=https://web.archive.org/web/20080822041214/http://nobelprize.org/nobelfoundation/publications/lectures/index.html |date=August 22, 2008 }}</ref> Mechnikov was awarded the 1908 [[Nobel Prize in Physiology or Medicine]] for his discovery.<ref name=Paul>{{cite journal|title=Ilya Ilich Metchnikoff (1845–1915) and Paul Ehrlich (1854–1915): the centennial of the 1908 Nobel Prize in Physiology or Medicine|journal=Journal of Medical Biography|year=2008|first=FC|last=Schmalstieg|author2=AS Goldman|volume=16|issue=2|pages=96–103|pmid=18463079|doi=10.1258/jmb.2008.008006|s2cid=25063709}}</ref> Phagocytes occur in many species; some [[amoeboid|amoebae]] behave like macrophage phagocytes, which suggests that phagocytes appeared early in the evolution of life.<ref name=amoebaphage>Janeway, Chapter: [https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=phagocytes,evolution&rid=imm.section.2367#2368 Evolution of the innate immune system.] retrieved on March 20, 2009</ref>',
6 => '',
7 => 'Phagocytes of humans and other animals are called "professional" or "non-professional" depending on how effective they are at [[phagocytosis]].<ref name=Ernst186>{{Harvnb|Ernst|Stendahl|2006|p=186}}</ref> The professional phagocytes include many types of [[white blood cell]]s (such as [[neutrophil]]s, [[monocyte]]s, [[macrophage]]s, [[mast cell]]s, and [[dendritic cell]]s).<ref name=Rob>{{Harvnb|Robinson|Babcock|1998|p=187}} and {{Harvnb|Ernst|Stendahl|2006|pp=7–10}}</ref> The main difference between professional and non-professional phagocytes is that the professional phagocytes have molecules called [[receptor (biochemistry)|receptors]] on their surfaces that can detect harmful objects, such as bacteria, that are not normally found in the body.<ref name= something>{{Harvnb|Ernst|Stendahl|2006|p=10}}</ref> Phagocytes are crucial in fighting infections, as well as in maintaining healthy tissues by removing dead and dying cells that have reached the end of their lifespan.<ref name="pathogenesis"/>',
8 => '',
9 => 'During an infection, chemical signals attract phagocytes to places where the pathogen has invaded the body. These chemicals may come from bacteria or from other phagocytes already present. The phagocytes move by a method called [[chemotaxis]]. When phagocytes come into contact with bacteria, the receptors on the phagocyte's surface will bind to them. This binding will lead to the engulfing of the bacteria by the phagocyte.<ref name=money/> Some phagocytes kill the ingested pathogen with [[reactive oxygen species|oxidants]] and [[nitric oxide]].<ref name=pmid15378046>{{cite journal |author=Fang FC |title=Antimicrobial reactive oxygen and nitrogen species: concepts and controversies |journal=Nat. Rev. Microbiol. |volume=2 |issue=10 |pages=820–32 |date=October 2004 |pmid=15378046 |doi=10.1038/nrmicro1004 |s2cid=11063073 }}</ref> After phagocytosis, macrophages and dendritic cells can also participate in [[antigen presentation]], a process in which a phagocyte moves parts of the ingested material back to its surface. This material is then displayed to other cells of the immune system. Some phagocytes then travel to the body's [[lymph node]]s and display the material to white blood cells called [[lymphocytes]]. This process is important in building immunity,<ref name=ATP>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=172–84}}</ref> and many pathogens have evolved methods to evade attacks by phagocytes.<ref name=USC/>',
10 => '',
11 => '== History ==',
12 => '[[File:Professeur Metchnikoff, portrait du scientifique dans un laboratoire de recherche.jpg|thumb|Ilya Ilyich Mechnikov in his laboratory|alt=A bearded old man holding up a test tube. He is sitting at a table by a window. The table is covered with many small bottles and test tubes.]]',
13 => 'The Russian zoologist [[Ilya Ilyich Mechnikov]] (1845–1916) first recognized that specialized cells were involved in defense against microbial infections.<ref name="pmid31001278">{{cite journal |vauthors=Kaufmann SH|title=Immunology's Coming of Age |journal=Frontiers in Immunology |volume=10 |pages=684 |date=2019 |pmid=31001278 |pmc=6456699 |doi=10.3389/fimmu.2019.00684 |doi-access=free }}</ref> In 1882, he studied [[motility|motile]] (freely moving) cells in the [[larva]]e of [[Sea star|starfishes]], believing they were important to the animals' immune defenses. To test his idea, he inserted small thorns from a [[tangerine]] tree into the larvae. After a few hours he noticed that the motile cells had surrounded the thorns.<ref name="pmid31001278"/> Mechnikov traveled to [[Vienna]] and shared his ideas with [[Carl Friedrich Wilhelm Claus|Carl Friedrich Claus]] who suggested the name "phagocyte" (from the Greek words ''{{lang|grc-Latn|phagein}}'', meaning "to eat or devour", and ''{{lang|grc-Latn|kutos}}'', meaning "hollow vessel"<ref name=ox />) for the cells that Mechnikov had observed.<ref name="pmid9544583">{{cite journal | author = Aterman K | title = Medals, memoirs—and Metchnikoff | journal = J. Leukoc. Biol. | volume = 63 | issue = 4 | pages = 515–17 | date = April 1, 1998 | pmid = 9544583 | doi = 10.1002/jlb.63.4.515 | s2cid = 44748502 | doi-access = free }}</ref>',
14 => '',
15 => 'A year later, Mechnikov studied a fresh water [[crustacean]] called ''[[Daphnia]]'', a tiny transparent animal that can be examined directly under a microscope. He discovered that fungal spores that attacked the animal were destroyed by phagocytes. He went on to extend his observations to the white blood cells of mammals and discovered that the bacterium ''[[Bacillus anthracis]]'' could be engulfed and killed by phagocytes, a process that he called [[phagocytosis]].<ref name=autogenerated5>{{cite web|url=http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html|title=Ilya Mechnikov|publisher=The Nobel Foundation|access-date=December 19, 2014}}</ref> Mechnikov proposed that phagocytes were a primary defense against invading organisms.<ref name="pmid31001278"/>',
16 => '',
17 => 'In 1903, [[Almroth Wright]] discovered that phagocytosis was reinforced by specific [[antibody|antibodies]] that he called [[opsonin]]s, from the Greek ''[[opson]]'', "a dressing or relish".<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|p=263}}</ref> Mechnikov was awarded (jointly with [[Paul Ehrlich]]) the 1908 [[Nobel Prize in Physiology or Medicine]] for his work on phagocytes and phagocytosis.<ref name= Paul/>',
18 => '',
19 => 'Although the importance of these discoveries slowly gained acceptance during the early twentieth century, the intricate relationships between phagocytes and all the other components of the immune system were not known until the 1980s.<ref>{{Harvnb|Robinson|Babcock|1998|p=vii}}</ref>',
20 => '',
21 => '== Phagocytosis ==',
22 => '{{main|Phagocytosis}}',
23 => '[[File:Phagocytosis in three steps.png|thumb|Phagocytosis in three steps: 1. Unbound phagocyte surface receptors do not trigger phagocytosis. 2. Binding of receptors causes them to cluster. 3. Phagocytosis is triggered and the particle is taken up by the phagocyte.|alt=A cartoon: 1. The particle is depicted by an oval and the surface of the phagocyte by a straight line. Different smaller shapes are on the line and the oval. 2. The smaller particles on each surface join. 3. The line is now concave and partially wraps around the oval.]]',
24 => 'Phagocytosis is the process of taking in particles such as bacteria, invasive [[fungi]], parasites, [[apoptosis|dead host cells]], and cellular and foreign debris by a cell.<ref name=superman2>{{Harvnb|Ernst|Stendahl|2006|p=4}}</ref> It involves a chain of molecular processes.<ref>{{Harvnb|Ernst|Stendahl|2006|p=78}}</ref><ref name="pmid29727727">{{cite journal |vauthors=Feldman MB, Vyas JM, Mansour MK |title=It takes a village: Phagocytes play a central role in fungal immunity |journal=Seminars in Cell & Developmental Biology |volume=89 |issue= |pages=16–23 |date=May 2019 |pmid=29727727 |pmc=6235731 |doi=10.1016/j.semcdb.2018.04.008}}</ref> Phagocytosis occurs after the foreign body, a bacterial cell, for example, has bound to molecules called "receptors" that are on the surface of the phagocyte. The phagocyte then stretches itself around the bacterium and engulfs it. Phagocytosis of bacteria by human neutrophils takes on average nine minutes.<ref name="pmid8301210">{{cite journal | author = Hampton MB, Vissers MC, Winterbourn CC | title = A single assay for measuring the rates of phagocytosis and bacterial killing by neutrophils | journal = J. Leukoc. Biol. | volume = 55 | issue = 2 | pages = 147–52 | date = February 1994 | pmid = 8301210 | doi = 10.1002/jlb.55.2.147| url = http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210 | archive-url = https://archive.today/20121228084302/http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210 | url-status = dead | archive-date = December 28, 2012 | last2 = Vissers | last3 = Winterbourn | s2cid = 44911791 | access-date = December 19, 2014 }}</ref> Once inside this phagocyte, the bacterium is trapped in a compartment called a [[phagosome]]. Within one minute the phagosome merges with either a [[lysosome]] or a [[Granule (cell biology)|granule]] to form a [[phagolysosome]]. The bacterium is then subjected to an overwhelming array of killing mechanisms<ref>{{Harvnb|Delves|Martin|Burton|Roit|2006|pp=6–7}}</ref> and is dead a few minutes later.<ref name="pmid8301210"/> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref> Phagocytes have voracious appetites; scientists have even fed macrophages with [[iron filings]] and then used a small magnet to separate them from other cells.<ref>{{Harvnb|Sompayrac|2019|p=2}}</ref>'
] |
All external links added in the edit (added_links) | [] |
All external links removed in the edit (removed_links) | [
0 => '//doi.org/10.1002%2Fjlb.55.2.147',
1 => '//doi.org/10.1002%2Fjlb.63.4.515',
2 => '//doi.org/10.1016%2Fj.semcdb.2018.04.008',
3 => '//doi.org/10.1038%2Fnrmicro1004',
4 => '//doi.org/10.1258%2Fjmb.2008.008006',
5 => '//doi.org/10.3389%2Ffimmu.2019.00684',
6 => '//pubmed.ncbi.nlm.nih.gov/15378046',
7 => '//pubmed.ncbi.nlm.nih.gov/18463079',
8 => '//pubmed.ncbi.nlm.nih.gov/29727727',
9 => '//pubmed.ncbi.nlm.nih.gov/31001278',
10 => '//pubmed.ncbi.nlm.nih.gov/8301210',
11 => '//pubmed.ncbi.nlm.nih.gov/9544583',
12 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC6456699',
13 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC6235731',
14 => 'http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html',
15 => 'http://nobelprize.org/nobelfoundation/publications/lectures/index.html',
16 => 'http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210',
17 => 'https://api.semanticscholar.org/CorpusID:25063709',
18 => 'https://api.semanticscholar.org/CorpusID:11063073',
19 => 'https://api.semanticscholar.org/CorpusID:44748502',
20 => 'https://api.semanticscholar.org/CorpusID:44911791',
21 => 'https://archive.today/20121228084302/http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210',
22 => 'https://web.archive.org/web/20080822041214/http://nobelprize.org/nobelfoundation/publications/lectures/index.html',
23 => 'https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=phagocytes,evolution&rid=imm.section.2367#2368'
] |
All external links in the new text (all_links) | [
0 => '//doi.org/10.1182%2Fblood-2007-12-077917',
1 => '//pubmed.ncbi.nlm.nih.gov/18684880',
2 => 'https://api.semanticscholar.org/CorpusID:746699',
3 => '//doi.org/10.1016%2FS0022-1759(99)00146-5',
4 => '//pubmed.ncbi.nlm.nih.gov/10618505',
5 => '//doi.org/10.1016%2FS1357-2725(96)00084-2',
6 => '//pubmed.ncbi.nlm.nih.gov/9022278',
7 => '//doi.org/10.1111%2Fpaa.1999.111.5.383',
8 => '//pubmed.ncbi.nlm.nih.gov/10519157',
9 => '//doi.org/10.1016%2Fj.lab.2004.05.014',
10 => '//pubmed.ncbi.nlm.nih.gov/15478278',
11 => '//doi.org/10.1189%2Fjlb.0603252',
12 => '//pubmed.ncbi.nlm.nih.gov/14525967',
13 => 'https://api.semanticscholar.org/CorpusID:15862242',
14 => '//pubmed.ncbi.nlm.nih.gov/18846805',
15 => '//doi.org/10.1097%2FMOH.0b013e3282f2bcce',
16 => '//pubmed.ncbi.nlm.nih.gov/18043242',
17 => 'https://api.semanticscholar.org/CorpusID:43243529',
18 => '//doi.org/10.1590%2Fs1413-86702007000500010',
19 => '//pubmed.ncbi.nlm.nih.gov/17962876',
20 => 'https://ui.adsabs.harvard.edu/abs/1995Sci...267.1456T',
21 => '//doi.org/10.1126%2Fscience.7878464',
22 => '//pubmed.ncbi.nlm.nih.gov/7878464',
23 => 'https://api.semanticscholar.org/CorpusID:12991980',
24 => 'http://www.merriam-webster.com/dictionary/apoptosis',
25 => 'https://semanticscholar.org/paper/0946eda3ac2cb65b78a7af7b879f97db91c7023a',
26 => '//doi.org/10.1126%2Fscience.1087621',
27 => '//pubmed.ncbi.nlm.nih.gov/14645847',
28 => 'https://api.semanticscholar.org/CorpusID:36252352',
29 => '//doi.org/10.1016%2Fj.coi.2019.11.009',
30 => '//pubmed.ncbi.nlm.nih.gov/31837595',
31 => 'https://semanticscholar.org/paper/ca6fd5581faa5fa9ee33ab1a2d993a910188788c',
32 => 'https://ui.adsabs.harvard.edu/abs/2003Sci...302.1563W',
33 => '//doi.org/10.1126%2Fscience.1087641',
34 => '//pubmed.ncbi.nlm.nih.gov/14645848',
35 => 'https://api.semanticscholar.org/CorpusID:25672278',
36 => 'https://semanticscholar.org/paper/da2238a1c09adaca71a04c8c04305a189db6c865',
37 => '//doi.org/10.1126%2Fscience.1092533',
38 => '//hdl.handle.net/1842%2F448',
39 => '//pubmed.ncbi.nlm.nih.gov/14645835',
40 => 'https://api.semanticscholar.org/CorpusID:13402617',
41 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3125982',
42 => '//doi.org/10.1016%2Fj.tcb.2008.08.002',
43 => '//pubmed.ncbi.nlm.nih.gov/18774293',
44 => 'https://web.archive.org/web/20080112211805/http://pim.medicine.dal.ca/apc.htm',
45 => 'http://pim.medicine.dal.ca/apc.htm',
46 => '//doi.org/10.1038%2Fsj.icb.7100088',
47 => '//pubmed.ncbi.nlm.nih.gov/17592494',
48 => 'https://api.semanticscholar.org/CorpusID:36342899',
49 => 'https://web.archive.org/web/20090311032056/http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php',
50 => 'http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php',
51 => '//doi.org/10.1007%2FBF02934736',
52 => '//pubmed.ncbi.nlm.nih.gov/17120464',
53 => 'https://api.semanticscholar.org/CorpusID:27585046',
54 => 'https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=migration&rid=imm.section.203#206',
55 => '//doi.org/10.1016%2FS0955-0674(03)00103-0',
56 => '//pubmed.ncbi.nlm.nih.gov/14519390',
57 => '//doi.org/10.1111%2Fj.1440-1827.1996.tb03641.x',
58 => '//pubmed.ncbi.nlm.nih.gov/8870002',
59 => 'https://api.semanticscholar.org/CorpusID:6049656',
60 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC1470168',
61 => '//doi.org/10.2307%2F3433544',
62 => '//www.jstor.org/stable/3433544',
63 => '//pubmed.ncbi.nlm.nih.gov/9400735',
64 => 'https://web.archive.org/web/20101231014453/http://nic.sav.sk/logos/books/scientific/node15.html',
65 => 'http://nic.sav.sk/logos/books/scientific/node15.html',
66 => '//doi.org/10.1203%2F00006450-199812000-00021',
67 => '//pubmed.ncbi.nlm.nih.gov/9853933',
68 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2276935',
69 => '//doi.org/10.1111%2Fj.1365-2249.2007.03532.x',
70 => '//pubmed.ncbi.nlm.nih.gov/17991288',
71 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2532980',
72 => '//doi.org/10.1172%2FJCI35740',
73 => '//pubmed.ncbi.nlm.nih.gov/18787642',
74 => '//doi.org/10.1038%2Fnri.2017.105',
75 => '//pubmed.ncbi.nlm.nih.gov/28990587',
76 => 'https://api.semanticscholar.org/CorpusID:25067858',
77 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2139237',
78 => '//doi.org/10.1084%2Fjem.137.5.1142',
79 => '//pubmed.ncbi.nlm.nih.gov/4573839',
80 => 'http://www.rockefeller.edu/labheads/steinman/steinman-lab.php',
81 => '//doi.org/10.1146%2Fannurev.immunol.20.100301.064828',
82 => '//pubmed.ncbi.nlm.nih.gov/11861614',
83 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3240143',
84 => '//doi.org/10.1186%2Far567',
85 => '//pubmed.ncbi.nlm.nih.gov/12110131',
86 => 'https://www.karger.com/Article/PDF/000232565',
87 => '//doi.org/10.1159%2F000232565',
88 => '//pubmed.ncbi.nlm.nih.gov/19672091',
89 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2856637',
90 => '//doi.org/10.1038%2Fni.f.216',
91 => '//pubmed.ncbi.nlm.nih.gov/18936782',
92 => '//doi.org/10.1034%2Fj.1600-065X.2001.790102.x',
93 => '//pubmed.ncbi.nlm.nih.gov/11292019',
94 => 'https://api.semanticscholar.org/CorpusID:23115222',
95 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC38514',
96 => 'https://ui.adsabs.harvard.edu/abs/1996PNAS...93.9827C',
97 => '//doi.org/10.1073%2Fpnas.93.18.9827',
98 => '//pubmed.ncbi.nlm.nih.gov/8790416',
99 => 'http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=8568252',
100 => '//pubmed.ncbi.nlm.nih.gov/8568252',
101 => '//doi.org/10.2500%2F108854101778148764',
102 => '//pubmed.ncbi.nlm.nih.gov/11424870',
103 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3343118',
104 => '//doi.org/10.1371%2Fjournal.ppat.1002619',
105 => '//pubmed.ncbi.nlm.nih.gov/22577358',
106 => '//doi.org/10.1038%2Fcdd.2008.58',
107 => '//pubmed.ncbi.nlm.nih.gov/18451871',
108 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC97802',
109 => '//doi.org/10.1128%2FIAI.68.12.6939-6945.2000',
110 => '//pubmed.ncbi.nlm.nih.gov/11083817',
111 => '//doi.org/10.1242%2Fjcs.114.1.119',
112 => '//pubmed.ncbi.nlm.nih.gov/11112696',
113 => '//doi.org/10.1016%2FS0962-8924(00)88955-2',
114 => '//pubmed.ncbi.nlm.nih.gov/14732160',
115 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC5732227',
116 => '//doi.org/10.3389%2Ffimmu.2017.01781',
117 => '//pubmed.ncbi.nlm.nih.gov/29321780',
118 => 'http://textbookofbacteriology.net/antiphago.html',
119 => 'http://jcs.biologists.org/cgi/pmidlookup?view=long&pmid=10462516',
120 => '//doi.org/10.1242%2Fjcs.112.18.2993',
121 => '//pubmed.ncbi.nlm.nih.gov/10462516',
122 => '//doi.org/10.1016%2FS0966-842X(02)02343-0',
123 => '//pubmed.ncbi.nlm.nih.gov/11973157',
124 => '//doi.org/10.1016%2Fj.yexcr.2005.05.024',
125 => '//pubmed.ncbi.nlm.nih.gov/15992798',
126 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC96650',
127 => '//doi.org/10.1128%2FIAI.67.8.3757-3762.1999',
128 => '//pubmed.ncbi.nlm.nih.gov/10417134',
129 => '//doi.org/10.1074%2Fjbc.M411374200',
130 => '//pubmed.ncbi.nlm.nih.gov/15501828',
131 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2632042',
132 => '//doi.org/10.1128%2FIAI.01186-08',
133 => '//pubmed.ncbi.nlm.nih.gov/19047408',
134 => '//doi.org/10.1038%2Fnrmicro1289',
135 => '//pubmed.ncbi.nlm.nih.gov/16322743',
136 => 'https://api.semanticscholar.org/CorpusID:205496221',
137 => '//doi.org/10.1078%2F1438-4221-00159',
138 => '//pubmed.ncbi.nlm.nih.gov/11890550',
139 => '//doi.org/10.1006%2Fsmim.2001.0335',
140 => '//pubmed.ncbi.nlm.nih.gov/11708894',
141 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC1171211',
142 => '//doi.org/10.1093%2Femboj%2F18.5.1199',
143 => '//pubmed.ncbi.nlm.nih.gov/10064587',
144 => '//doi.org/10.1016%2FS0966-842X(98)01324-9',
145 => '//pubmed.ncbi.nlm.nih.gov/9807783',
146 => '//doi.org/10.1007%2Fs00011-007-7206-z',
147 => '//pubmed.ncbi.nlm.nih.gov/18607538',
148 => 'https://api.semanticscholar.org/CorpusID:22127111',
149 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC1951982',
150 => '//doi.org/10.1128%2FIAI.01779-06',
151 => '//pubmed.ncbi.nlm.nih.gov/17517863',
152 => '//doi.org/10.1111%2Fj.1365-2958.2005.04583.x',
153 => '//pubmed.ncbi.nlm.nih.gov/15819624',
154 => 'https://api.semanticscholar.org/CorpusID:14748436',
155 => '//doi.org/10.1016%2Fj.jdermsci.2006.03.011',
156 => '//pubmed.ncbi.nlm.nih.gov/16679003',
157 => '//doi.org/10.1016%2Fj.pt.2004.10.004',
158 => '//pubmed.ncbi.nlm.nih.gov/15639739',
159 => '//doi.org/10.1017%2FS0031182005008139',
160 => '//pubmed.ncbi.nlm.nih.gov/16281989',
161 => 'https://api.semanticscholar.org/CorpusID:24696519',
162 => '//doi.org/10.1016%2FS0272-6386(99)70375-6',
163 => '//pubmed.ncbi.nlm.nih.gov/10430993',
164 => '//doi.org/10.1097%2F00075198-200102000-00001',
165 => '//pubmed.ncbi.nlm.nih.gov/11373504',
166 => 'https://api.semanticscholar.org/CorpusID:24164360',
167 => '//doi.org/10.1097%2F01.moh.0000190113.31027.d5',
168 => '//pubmed.ncbi.nlm.nih.gov/16319683',
169 => 'https://api.semanticscholar.org/CorpusID:29374195',
170 => 'https://semanticscholar.org/paper/33d1bbeddab0d02bbd37634dab1e745258500732',
171 => '//doi.org/10.1097%2F01.CCM.0000057843.47705.E8',
172 => '//pubmed.ncbi.nlm.nih.gov/12682440',
173 => 'https://api.semanticscholar.org/CorpusID:4004607',
174 => 'https://ui.adsabs.harvard.edu/abs/1997NYASA.832..426R',
175 => '//doi.org/10.1111%2Fj.1749-6632.1997.tb46269.x',
176 => '//pubmed.ncbi.nlm.nih.gov/9704069',
177 => 'https://api.semanticscholar.org/CorpusID:10318084',
178 => 'https://biblio.ugent.be/publication/369324',
179 => 'https://ui.adsabs.harvard.edu/abs/2006NYASA1081..130C',
180 => '//doi.org/10.1196%2Fannals.1373.014',
181 => '//hdl.handle.net/1854%2FLU-369324',
182 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC7168046',
183 => '//pubmed.ncbi.nlm.nih.gov/17135502',
184 => '//doi.org/10.1016%2Fj.mib.2008.05.005',
185 => '//pubmed.ncbi.nlm.nih.gov/18550419',
186 => '//doi.org/10.1016%2FS1937-6448(08)01206-9',
187 => '//pubmed.ncbi.nlm.nih.gov/19081545',
188 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3291017',
189 => 'https://ui.adsabs.harvard.edu/abs/2007Sci...317..678C',
190 => '//doi.org/10.1126%2Fscience.1143991',
191 => '//pubmed.ncbi.nlm.nih.gov/17673666',
192 => '//doi.org/10.1016%2Fj.dci.2008.11.004',
193 => '//pubmed.ncbi.nlm.nih.gov/19063916',
194 => 'http://www.cambridge.org/9780521845694',
195 => 'https://archive.org/details/phagocytefunctio0000unse',
196 => 'https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes&library=OLBP',
197 => 'https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes',
198 => 'https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes&library=0CHOOSE0',
199 => 'https://meshb.nlm.nih.gov/record/ui?name=Phagocytes',
200 => 'https://www.youtube.com/watch?v=JnlULOjUhSQ'
] |
Links in the page, before the edit (old_links) | [
0 => '//doi.org/10.1002%2Fjlb.55.2.147',
1 => '//doi.org/10.1002%2Fjlb.63.4.515',
2 => '//doi.org/10.1006%2Fsmim.2001.0335',
3 => '//doi.org/10.1007%2FBF02934736',
4 => '//doi.org/10.1007%2Fs00011-007-7206-z',
5 => '//doi.org/10.1016%2FS0022-1759(99)00146-5',
6 => '//doi.org/10.1016%2FS0272-6386(99)70375-6',
7 => '//doi.org/10.1016%2FS0955-0674(03)00103-0',
8 => '//doi.org/10.1016%2FS0962-8924(00)88955-2',
9 => '//doi.org/10.1016%2FS0966-842X(02)02343-0',
10 => '//doi.org/10.1016%2FS0966-842X(98)01324-9',
11 => '//doi.org/10.1016%2FS1357-2725(96)00084-2',
12 => '//doi.org/10.1016%2FS1937-6448(08)01206-9',
13 => '//doi.org/10.1016%2Fj.coi.2019.11.009',
14 => '//doi.org/10.1016%2Fj.dci.2008.11.004',
15 => '//doi.org/10.1016%2Fj.jdermsci.2006.03.011',
16 => '//doi.org/10.1016%2Fj.lab.2004.05.014',
17 => '//doi.org/10.1016%2Fj.mib.2008.05.005',
18 => '//doi.org/10.1016%2Fj.pt.2004.10.004',
19 => '//doi.org/10.1016%2Fj.semcdb.2018.04.008',
20 => '//doi.org/10.1016%2Fj.tcb.2008.08.002',
21 => '//doi.org/10.1016%2Fj.yexcr.2005.05.024',
22 => '//doi.org/10.1017%2FS0031182005008139',
23 => '//doi.org/10.1034%2Fj.1600-065X.2001.790102.x',
24 => '//doi.org/10.1038%2Fcdd.2008.58',
25 => '//doi.org/10.1038%2Fni.f.216',
26 => '//doi.org/10.1038%2Fnri.2017.105',
27 => '//doi.org/10.1038%2Fnrmicro1004',
28 => '//doi.org/10.1038%2Fnrmicro1289',
29 => '//doi.org/10.1038%2Fsj.icb.7100088',
30 => '//doi.org/10.1073%2Fpnas.93.18.9827',
31 => '//doi.org/10.1074%2Fjbc.M411374200',
32 => '//doi.org/10.1078%2F1438-4221-00159',
33 => '//doi.org/10.1084%2Fjem.137.5.1142',
34 => '//doi.org/10.1093%2Femboj%2F18.5.1199',
35 => '//doi.org/10.1097%2F00075198-200102000-00001',
36 => '//doi.org/10.1097%2F01.CCM.0000057843.47705.E8',
37 => '//doi.org/10.1097%2F01.moh.0000190113.31027.d5',
38 => '//doi.org/10.1097%2FMOH.0b013e3282f2bcce',
39 => '//doi.org/10.1111%2Fj.1365-2249.2007.03532.x',
40 => '//doi.org/10.1111%2Fj.1365-2958.2005.04583.x',
41 => '//doi.org/10.1111%2Fj.1440-1827.1996.tb03641.x',
42 => '//doi.org/10.1111%2Fj.1749-6632.1997.tb46269.x',
43 => '//doi.org/10.1111%2Fpaa.1999.111.5.383',
44 => '//doi.org/10.1126%2Fscience.1087621',
45 => '//doi.org/10.1126%2Fscience.1087641',
46 => '//doi.org/10.1126%2Fscience.1092533',
47 => '//doi.org/10.1126%2Fscience.1143991',
48 => '//doi.org/10.1126%2Fscience.7878464',
49 => '//doi.org/10.1128%2FIAI.01186-08',
50 => '//doi.org/10.1128%2FIAI.01779-06',
51 => '//doi.org/10.1128%2FIAI.67.8.3757-3762.1999',
52 => '//doi.org/10.1128%2FIAI.68.12.6939-6945.2000',
53 => '//doi.org/10.1146%2Fannurev.immunol.20.100301.064828',
54 => '//doi.org/10.1159%2F000232565',
55 => '//doi.org/10.1172%2FJCI35740',
56 => '//doi.org/10.1182%2Fblood-2007-12-077917',
57 => '//doi.org/10.1186%2Far567',
58 => '//doi.org/10.1189%2Fjlb.0603252',
59 => '//doi.org/10.1196%2Fannals.1373.014',
60 => '//doi.org/10.1203%2F00006450-199812000-00021',
61 => '//doi.org/10.1242%2Fjcs.112.18.2993',
62 => '//doi.org/10.1242%2Fjcs.114.1.119',
63 => '//doi.org/10.1258%2Fjmb.2008.008006',
64 => '//doi.org/10.1371%2Fjournal.ppat.1002619',
65 => '//doi.org/10.1590%2Fs1413-86702007000500010',
66 => '//doi.org/10.2307%2F3433544',
67 => '//doi.org/10.2500%2F108854101778148764',
68 => '//doi.org/10.3389%2Ffimmu.2017.01781',
69 => '//doi.org/10.3389%2Ffimmu.2019.00684',
70 => '//hdl.handle.net/1842%2F448',
71 => '//hdl.handle.net/1854%2FLU-369324',
72 => '//pubmed.ncbi.nlm.nih.gov/10064587',
73 => '//pubmed.ncbi.nlm.nih.gov/10417134',
74 => '//pubmed.ncbi.nlm.nih.gov/10430993',
75 => '//pubmed.ncbi.nlm.nih.gov/10462516',
76 => '//pubmed.ncbi.nlm.nih.gov/10519157',
77 => '//pubmed.ncbi.nlm.nih.gov/10618505',
78 => '//pubmed.ncbi.nlm.nih.gov/11083817',
79 => '//pubmed.ncbi.nlm.nih.gov/11112696',
80 => '//pubmed.ncbi.nlm.nih.gov/11292019',
81 => '//pubmed.ncbi.nlm.nih.gov/11373504',
82 => '//pubmed.ncbi.nlm.nih.gov/11424870',
83 => '//pubmed.ncbi.nlm.nih.gov/11708894',
84 => '//pubmed.ncbi.nlm.nih.gov/11861614',
85 => '//pubmed.ncbi.nlm.nih.gov/11890550',
86 => '//pubmed.ncbi.nlm.nih.gov/11973157',
87 => '//pubmed.ncbi.nlm.nih.gov/12110131',
88 => '//pubmed.ncbi.nlm.nih.gov/12682440',
89 => '//pubmed.ncbi.nlm.nih.gov/14519390',
90 => '//pubmed.ncbi.nlm.nih.gov/14525967',
91 => '//pubmed.ncbi.nlm.nih.gov/14645835',
92 => '//pubmed.ncbi.nlm.nih.gov/14645847',
93 => '//pubmed.ncbi.nlm.nih.gov/14645848',
94 => '//pubmed.ncbi.nlm.nih.gov/14732160',
95 => '//pubmed.ncbi.nlm.nih.gov/15378046',
96 => '//pubmed.ncbi.nlm.nih.gov/15478278',
97 => '//pubmed.ncbi.nlm.nih.gov/15501828',
98 => '//pubmed.ncbi.nlm.nih.gov/15639739',
99 => '//pubmed.ncbi.nlm.nih.gov/15819624',
100 => '//pubmed.ncbi.nlm.nih.gov/15992798',
101 => '//pubmed.ncbi.nlm.nih.gov/16281989',
102 => '//pubmed.ncbi.nlm.nih.gov/16319683',
103 => '//pubmed.ncbi.nlm.nih.gov/16322743',
104 => '//pubmed.ncbi.nlm.nih.gov/16679003',
105 => '//pubmed.ncbi.nlm.nih.gov/17120464',
106 => '//pubmed.ncbi.nlm.nih.gov/17135502',
107 => '//pubmed.ncbi.nlm.nih.gov/17517863',
108 => '//pubmed.ncbi.nlm.nih.gov/17592494',
109 => '//pubmed.ncbi.nlm.nih.gov/17673666',
110 => '//pubmed.ncbi.nlm.nih.gov/17962876',
111 => '//pubmed.ncbi.nlm.nih.gov/17991288',
112 => '//pubmed.ncbi.nlm.nih.gov/18043242',
113 => '//pubmed.ncbi.nlm.nih.gov/18451871',
114 => '//pubmed.ncbi.nlm.nih.gov/18463079',
115 => '//pubmed.ncbi.nlm.nih.gov/18550419',
116 => '//pubmed.ncbi.nlm.nih.gov/18607538',
117 => '//pubmed.ncbi.nlm.nih.gov/18684880',
118 => '//pubmed.ncbi.nlm.nih.gov/18774293',
119 => '//pubmed.ncbi.nlm.nih.gov/18787642',
120 => '//pubmed.ncbi.nlm.nih.gov/18846805',
121 => '//pubmed.ncbi.nlm.nih.gov/18936782',
122 => '//pubmed.ncbi.nlm.nih.gov/19047408',
123 => '//pubmed.ncbi.nlm.nih.gov/19063916',
124 => '//pubmed.ncbi.nlm.nih.gov/19081545',
125 => '//pubmed.ncbi.nlm.nih.gov/19672091',
126 => '//pubmed.ncbi.nlm.nih.gov/22577358',
127 => '//pubmed.ncbi.nlm.nih.gov/28990587',
128 => '//pubmed.ncbi.nlm.nih.gov/29321780',
129 => '//pubmed.ncbi.nlm.nih.gov/29727727',
130 => '//pubmed.ncbi.nlm.nih.gov/31001278',
131 => '//pubmed.ncbi.nlm.nih.gov/31837595',
132 => '//pubmed.ncbi.nlm.nih.gov/4573839',
133 => '//pubmed.ncbi.nlm.nih.gov/7878464',
134 => '//pubmed.ncbi.nlm.nih.gov/8301210',
135 => '//pubmed.ncbi.nlm.nih.gov/8568252',
136 => '//pubmed.ncbi.nlm.nih.gov/8790416',
137 => '//pubmed.ncbi.nlm.nih.gov/8870002',
138 => '//pubmed.ncbi.nlm.nih.gov/9022278',
139 => '//pubmed.ncbi.nlm.nih.gov/9400735',
140 => '//pubmed.ncbi.nlm.nih.gov/9544583',
141 => '//pubmed.ncbi.nlm.nih.gov/9704069',
142 => '//pubmed.ncbi.nlm.nih.gov/9807783',
143 => '//pubmed.ncbi.nlm.nih.gov/9853933',
144 => '//www.jstor.org/stable/3433544',
145 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC1470168',
146 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC1171211',
147 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC1951982',
148 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2276935',
149 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2532980',
150 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2139237',
151 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2632042',
152 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC2856637',
153 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3125982',
154 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3240143',
155 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3291017',
156 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC38514',
157 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC3343118',
158 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC5732227',
159 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC6456699',
160 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC6235731',
161 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC7168046',
162 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC97802',
163 => '//www.ncbi.nlm.nih.gov/pmc/articles/PMC96650',
164 => 'http://jcs.biologists.org/cgi/pmidlookup?view=long&pmid=10462516',
165 => 'http://nic.sav.sk/logos/books/scientific/node15.html',
166 => 'http://nobelprize.org/nobel_prizes/medicine/laureates/1908/mechnikov-bio.html',
167 => 'http://nobelprize.org/nobelfoundation/publications/lectures/index.html',
168 => 'http://pim.medicine.dal.ca/apc.htm',
169 => 'http://textbookofbacteriology.net/antiphago.html',
170 => 'http://www.cambridge.org/9780521845694',
171 => 'http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=8568252',
172 => 'http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210',
173 => 'http://www.merriam-webster.com/dictionary/apoptosis',
174 => 'http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php',
175 => 'http://www.rockefeller.edu/labheads/steinman/steinman-lab.php',
176 => 'https://api.semanticscholar.org/CorpusID:25063709',
177 => 'https://api.semanticscholar.org/CorpusID:12991980',
178 => 'https://api.semanticscholar.org/CorpusID:11063073',
179 => 'https://api.semanticscholar.org/CorpusID:44748502',
180 => 'https://api.semanticscholar.org/CorpusID:44911791',
181 => 'https://api.semanticscholar.org/CorpusID:746699',
182 => 'https://api.semanticscholar.org/CorpusID:15862242',
183 => 'https://api.semanticscholar.org/CorpusID:43243529',
184 => 'https://api.semanticscholar.org/CorpusID:36252352',
185 => 'https://api.semanticscholar.org/CorpusID:25672278',
186 => 'https://api.semanticscholar.org/CorpusID:13402617',
187 => 'https://api.semanticscholar.org/CorpusID:36342899',
188 => 'https://api.semanticscholar.org/CorpusID:27585046',
189 => 'https://api.semanticscholar.org/CorpusID:6049656',
190 => 'https://api.semanticscholar.org/CorpusID:23115222',
191 => 'https://api.semanticscholar.org/CorpusID:205496221',
192 => 'https://api.semanticscholar.org/CorpusID:22127111',
193 => 'https://api.semanticscholar.org/CorpusID:14748436',
194 => 'https://api.semanticscholar.org/CorpusID:24164360',
195 => 'https://api.semanticscholar.org/CorpusID:29374195',
196 => 'https://api.semanticscholar.org/CorpusID:4004607',
197 => 'https://api.semanticscholar.org/CorpusID:10318084',
198 => 'https://api.semanticscholar.org/CorpusID:24696519',
199 => 'https://api.semanticscholar.org/CorpusID:25067858',
200 => 'https://archive.org/details/phagocytefunctio0000unse',
201 => 'https://archive.today/20121228084302/http://www.jleukbio.org/cgi/pmidlookup?view=long&pmid=8301210',
202 => 'https://biblio.ugent.be/publication/369324',
203 => 'https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes&library=OLBP',
204 => 'https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes',
205 => 'https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes&library=0CHOOSE0',
206 => 'https://meshb.nlm.nih.gov/record/ui?name=Phagocytes',
207 => 'https://semanticscholar.org/paper/0946eda3ac2cb65b78a7af7b879f97db91c7023a',
208 => 'https://semanticscholar.org/paper/33d1bbeddab0d02bbd37634dab1e745258500732',
209 => 'https://semanticscholar.org/paper/ca6fd5581faa5fa9ee33ab1a2d993a910188788c',
210 => 'https://semanticscholar.org/paper/da2238a1c09adaca71a04c8c04305a189db6c865',
211 => 'https://ui.adsabs.harvard.edu/abs/1995Sci...267.1456T',
212 => 'https://ui.adsabs.harvard.edu/abs/1996PNAS...93.9827C',
213 => 'https://ui.adsabs.harvard.edu/abs/1997NYASA.832..426R',
214 => 'https://ui.adsabs.harvard.edu/abs/2003Sci...302.1563W',
215 => 'https://ui.adsabs.harvard.edu/abs/2006NYASA1081..130C',
216 => 'https://ui.adsabs.harvard.edu/abs/2007Sci...317..678C',
217 => 'https://web.archive.org/web/20080112211805/http://pim.medicine.dal.ca/apc.htm',
218 => 'https://web.archive.org/web/20080822041214/http://nobelprize.org/nobelfoundation/publications/lectures/index.html',
219 => 'https://web.archive.org/web/20090311032056/http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php',
220 => 'https://web.archive.org/web/20101231014453/http://nic.sav.sk/logos/books/scientific/node15.html',
221 => 'https://www.karger.com/Article/PDF/000232565',
222 => 'https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=phagocytes,evolution&rid=imm.section.2367#2368',
223 => 'https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=migration&rid=imm.section.203#206',
224 => 'https://www.youtube.com/watch?v=JnlULOjUhSQ'
] |
Parsed HTML source of the new revision (new_html) | '<div class="mw-parser-output"><p>hc3r;iwfghnhktbucu6vhiwer,kpohitv6wuiold;o3pk'oweruisd0[5jiiiiiiii#]4[=l Once inside this phagocyte, the bacterium is trapped in a compartment called a <a href="/enwiki/wiki/Phagosome" title="Phagosome">phagosome</a>. Within one minute the phagosome merges with either a <a href="/enwiki/wiki/Lysosome" title="Lysosome">lysosome</a> or a <a href="/enwiki/wiki/Granule_(cell_biology)" title="Granule (cell biology)">granule</a> to form a <a href="/enwiki/wiki/Phagolysosome" title="Phagolysosome">phagolysosome</a>. The bacterium is then subjected to an overwhelming array of killing mechanisms<sup id="cite_ref-1" class="reference"><a href="#cite_note-1">[1]</a></sup> and is dead a few minutes later.<sup id="cite_ref-pmid8301210_2-0" class="reference"><a href="#cite_note-pmid8301210-2">[2]</a></sup> Dendritic cells and macrophages are not so fast, and phagocytosis can take many hours in these cells. Macrophages are slow and untidy eaters; they engulf huge quantities of material and frequently release some undigested back into the tissues. This debris serves as a signal to recruit more phagocytes from the blood.<sup id="cite_ref-3" class="reference"><a href="#cite_note-3">[3]</a></sup> Phagocytes have voracious appetites; scientists have even fed macrophages with <a href="/enwiki/wiki/Iron_filings" title="Iron filings">iron filings</a> and then used a small magnet to separate them from other cells.<sup id="cite_ref-4" class="reference"><a href="#cite_note-4">[4]</a></sup>
</p>
<div class="thumb tleft"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Opsonin.png" class="image"><img alt="A cartoon: The macrophage is depicted as a distorted solid circle. On the surface of the circle is a small y-shaped figure that is connected to a solid rectangle that depicts a bacterium." src="/upwiki/wikipedia/commons/thumb/f/fd/Opsonin.png/220px-Opsonin.png" decoding="async" width="220" height="143" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/f/fd/Opsonin.png/330px-Opsonin.png 1.5x, /upwiki/wikipedia/commons/thumb/f/fd/Opsonin.png/440px-Opsonin.png 2x" data-file-width="859" data-file-height="560" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Opsonin.png" class="internal" title="Enlarge"></a></div>Macrophages have special receptors that enhance phagocytosis (not to scale)</div></div></div>
<p>A phagocyte has many types of receptors on its surface that are used to bind material.<sup id="cite_ref-USC_5-0" class="reference"><a href="#cite_note-USC-5">[5]</a></sup> They include <a href="/enwiki/wiki/Opsonin" title="Opsonin">opsonin</a> receptors, <a href="/enwiki/wiki/Scavenger_receptor_(immunology)" title="Scavenger receptor (immunology)">scavenger receptors</a>, and <a href="/enwiki/wiki/Toll-like_receptors" class="mw-redirect" title="Toll-like receptors">Toll-like receptors</a>. Opsonin receptors increase the phagocytosis of bacteria that have been coated with <a href="/enwiki/wiki/Immunoglobulin_G" title="Immunoglobulin G">immunoglobulin G</a> (IgG) <a href="/enwiki/wiki/Antibodies" class="mw-redirect" title="Antibodies">antibodies</a> or with <a href="/enwiki/wiki/Complement_system" title="Complement system">complement</a>. "Complement" is the name given to a complex series of protein molecules found in the blood that destroy cells or mark them for destruction.<sup id="cite_ref-6" class="reference"><a href="#cite_note-6">[6]</a></sup> Scavenger receptors bind to a large range of molecules on the surface of bacterial cells, and Toll-like receptors—so called because of their similarity to well-studied receptors in fruit flies that are encoded by the <a href="/enwiki/wiki/Toll_(gene)" class="mw-redirect" title="Toll (gene)">Toll gene</a>—bind to more specific molecules. Binding to Toll-like receptors increases phagocytosis and causes the phagocyte to release a group of hormones that cause <a href="/enwiki/wiki/Inflammation" title="Inflammation">inflammation</a>.<sup id="cite_ref-USC_5-1" class="reference"><a href="#cite_note-USC-5">[5]</a></sup>
</p>
<div id="toc" class="toc" role="navigation" aria-labelledby="mw-toc-heading"><input type="checkbox" role="button" id="toctogglecheckbox" class="toctogglecheckbox" style="display:none" /><div class="toctitle" lang="en" dir="ltr"><h2 id="mw-toc-heading">Contents</h2><span class="toctogglespan"><label class="toctogglelabel" for="toctogglecheckbox"></label></span></div>
<ul>
<li class="toclevel-1 tocsection-1"><a href="#Methods_of_killing"><span class="tocnumber">1</span> <span class="toctext">Methods of killing</span></a>
<ul>
<li class="toclevel-2 tocsection-2"><a href="#Oxygen-dependent_intracellular"><span class="tocnumber">1.1</span> <span class="toctext">Oxygen-dependent intracellular</span></a></li>
<li class="toclevel-2 tocsection-3"><a href="#Oxygen-independent_intracellular"><span class="tocnumber">1.2</span> <span class="toctext">Oxygen-independent intracellular</span></a></li>
<li class="toclevel-2 tocsection-4"><a href="#Extracellular"><span class="tocnumber">1.3</span> <span class="toctext">Extracellular</span></a></li>
<li class="toclevel-2 tocsection-5"><a href="#Viruses"><span class="tocnumber">1.4</span> <span class="toctext">Viruses</span></a></li>
</ul>
</li>
<li class="toclevel-1 tocsection-6"><a href="#Role_in_apoptosis"><span class="tocnumber">2</span> <span class="toctext">Role in apoptosis</span></a></li>
<li class="toclevel-1 tocsection-7"><a href="#Interactions_with_other_cells"><span class="tocnumber">3</span> <span class="toctext">Interactions with other cells</span></a>
<ul>
<li class="toclevel-2 tocsection-8"><a href="#Antigen_presentation"><span class="tocnumber">3.1</span> <span class="toctext">Antigen presentation</span></a></li>
<li class="toclevel-2 tocsection-9"><a href="#Immunological_tolerance"><span class="tocnumber">3.2</span> <span class="toctext">Immunological tolerance</span></a></li>
</ul>
</li>
<li class="toclevel-1 tocsection-10"><a href="#Professional_phagocytes"><span class="tocnumber">4</span> <span class="toctext">Professional phagocytes</span></a>
<ul>
<li class="toclevel-2 tocsection-11"><a href="#Activation"><span class="tocnumber">4.1</span> <span class="toctext">Activation</span></a></li>
<li class="toclevel-2 tocsection-12"><a href="#Migration"><span class="tocnumber">4.2</span> <span class="toctext">Migration</span></a></li>
<li class="toclevel-2 tocsection-13"><a href="#Monocytes"><span class="tocnumber">4.3</span> <span class="toctext">Monocytes</span></a></li>
<li class="toclevel-2 tocsection-14"><a href="#Macrophages"><span class="tocnumber">4.4</span> <span class="toctext">Macrophages</span></a></li>
<li class="toclevel-2 tocsection-15"><a href="#Neutrophils"><span class="tocnumber">4.5</span> <span class="toctext">Neutrophils</span></a></li>
<li class="toclevel-2 tocsection-16"><a href="#Dendritic_cells"><span class="tocnumber">4.6</span> <span class="toctext">Dendritic cells</span></a></li>
<li class="toclevel-2 tocsection-17"><a href="#Mast_cells"><span class="tocnumber">4.7</span> <span class="toctext">Mast cells</span></a></li>
</ul>
</li>
<li class="toclevel-1 tocsection-18"><a href="#Non-professional_phagocytes"><span class="tocnumber">5</span> <span class="toctext">Non-professional phagocytes</span></a></li>
<li class="toclevel-1 tocsection-19"><a href="#Pathogen_evasion_and_resistance"><span class="tocnumber">6</span> <span class="toctext">Pathogen evasion and resistance</span></a>
<ul>
<li class="toclevel-2 tocsection-20"><a href="#Avoiding_contact"><span class="tocnumber">6.1</span> <span class="toctext">Avoiding contact</span></a></li>
<li class="toclevel-2 tocsection-21"><a href="#Avoiding_engulfment"><span class="tocnumber">6.2</span> <span class="toctext">Avoiding engulfment</span></a></li>
<li class="toclevel-2 tocsection-22"><a href="#Survival_inside_the_phagocyte"><span class="tocnumber">6.3</span> <span class="toctext">Survival inside the phagocyte</span></a></li>
<li class="toclevel-2 tocsection-23"><a href="#Killing"><span class="tocnumber">6.4</span> <span class="toctext">Killing</span></a></li>
<li class="toclevel-2 tocsection-24"><a href="#Disruption_of_cell_signaling"><span class="tocnumber">6.5</span> <span class="toctext">Disruption of cell signaling</span></a></li>
</ul>
</li>
<li class="toclevel-1 tocsection-25"><a href="#Host_damage_by_phagocytes"><span class="tocnumber">7</span> <span class="toctext">Host damage by phagocytes</span></a></li>
<li class="toclevel-1 tocsection-26"><a href="#Evolutionary_origins"><span class="tocnumber">8</span> <span class="toctext">Evolutionary origins</span></a></li>
<li class="toclevel-1 tocsection-27"><a href="#References"><span class="tocnumber">9</span> <span class="toctext">References</span></a></li>
<li class="toclevel-1 tocsection-28"><a href="#External_links"><span class="tocnumber">10</span> <span class="toctext">External links</span></a></li>
</ul>
</div>
<h2><span class="mw-headline" id="Methods_of_killing">Methods of killing</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=1" title="Edit section: Methods of killing">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Phagocytosis2.png" class="image"><img alt="A cartoon that depicts the engulfment of a single bacterium, its passage through a cell where it is digested and released as debris." src="/upwiki/wikipedia/commons/thumb/e/e6/Phagocytosis2.png/220px-Phagocytosis2.png" decoding="async" width="220" height="155" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/e/e6/Phagocytosis2.png/330px-Phagocytosis2.png 1.5x, /upwiki/wikipedia/commons/thumb/e/e6/Phagocytosis2.png/440px-Phagocytosis2.png 2x" data-file-width="932" data-file-height="655" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Phagocytosis2.png" class="internal" title="Enlarge"></a></div>Simplified diagram of the phagocytosis and destruction of a bacterial cell</div></div></div>
<p>The killing of microbes is a critical function of phagocytes that is performed either within the phagocyte (<a href="/enwiki/wiki/Intracellular" class="mw-redirect" title="Intracellular">intracellular</a> killing) or outside of the phagocyte (<a href="/enwiki/wiki/Extracellular" class="mw-redirect" title="Extracellular">extracellular</a> killing).<sup id="cite_ref-pmid18684880_7-0" class="reference"><a href="#cite_note-pmid18684880-7">[7]</a></sup>
</p>
<h3><span class="mw-headline" id="Oxygen-dependent_intracellular">Oxygen-dependent intracellular</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=2" title="Edit section: Oxygen-dependent intracellular">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p>When a phagocyte ingests bacteria (or any material), its oxygen consumption increases. The increase in oxygen consumption, called a <a href="/enwiki/wiki/Respiratory_burst" title="Respiratory burst">respiratory burst</a>, produces reactive oxygen-containing molecules that are anti-microbial.<sup id="cite_ref-8" class="reference"><a href="#cite_note-8">[8]</a></sup> The oxygen compounds are toxic to both the invader and the cell itself, so they are kept in compartments inside the cell. This method of killing invading microbes by using the reactive oxygen-containing molecules is referred to as oxygen-dependent intracellular killing, of which there are two types.<sup id="cite_ref-pmid15378046_9-0" class="reference"><a href="#cite_note-pmid15378046-9">[9]</a></sup>
</p><p>The first type is the oxygen-dependent production of a <a href="/enwiki/wiki/Superoxide" title="Superoxide">superoxide</a>,<sup id="cite_ref-USC_5-2" class="reference"><a href="#cite_note-USC-5">[5]</a></sup> which is an oxygen-rich bacteria-killing substance.<sup id="cite_ref-10" class="reference"><a href="#cite_note-10">[10]</a></sup> The superoxide is converted to <a href="/enwiki/wiki/Hydrogen_peroxide" title="Hydrogen peroxide">hydrogen peroxide</a> and <a href="/enwiki/wiki/Singlet_oxygen" title="Singlet oxygen">singlet oxygen</a> by an enzyme called <a href="/enwiki/wiki/Superoxide_dismutase" title="Superoxide dismutase">superoxide dismutase</a>. Superoxides also react with the hydrogen peroxide to produce <a href="/enwiki/wiki/Hydroxyl_radicals" class="mw-redirect" title="Hydroxyl radicals">hydroxyl radicals</a>, which assist in killing the invading microbe.<sup id="cite_ref-USC_5-3" class="reference"><a href="#cite_note-USC-5">[5]</a></sup>
</p><p>The second type involves the use of the enzyme <a href="/enwiki/wiki/Myeloperoxidase" title="Myeloperoxidase">myeloperoxidase</a> from neutrophil granules.<sup id="cite_ref-pmid10519157_11-0" class="reference"><a href="#cite_note-pmid10519157-11">[11]</a></sup> When granules fuse with a phagosome, myeloperoxidase is released into the phagolysosome, and this enzyme uses hydrogen peroxide and <a href="/enwiki/wiki/Chlorine" title="Chlorine">chlorine</a> to create <a href="/enwiki/wiki/Hypochlorite" title="Hypochlorite">hypochlorite</a>, a substance used in domestic <a href="/enwiki/wiki/Bleach" title="Bleach">bleach</a>. Hypochlorite is extremely toxic to bacteria.<sup id="cite_ref-USC_5-4" class="reference"><a href="#cite_note-USC-5">[5]</a></sup> Myeloperoxidase contains a <a href="/enwiki/wiki/Heme" title="Heme">heme</a> pigment, which accounts for the green color of secretions rich in neutrophils, such as <a href="/enwiki/wiki/Pus" title="Pus">pus</a> and infected <a href="/enwiki/wiki/Sputum" title="Sputum">sputum</a>.<sup id="cite_ref-pmid15478278_12-0" class="reference"><a href="#cite_note-pmid15478278-12">[12]</a></sup>
</p>
<h3><span class="mw-headline" id="Oxygen-independent_intracellular">Oxygen-independent intracellular</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=3" title="Edit section: Oxygen-independent intracellular">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Gram-stain_of_gonorrhoea.jpg" class="image"><img alt="Pus under a microscope, there are many white blood cells with lobed nuclei. Inside some of the cells there are hundreds of bacteria that have been engulfed." src="/upwiki/wikipedia/commons/thumb/5/56/Gram-stain_of_gonorrhoea.jpg/220px-Gram-stain_of_gonorrhoea.jpg" decoding="async" width="220" height="135" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/5/56/Gram-stain_of_gonorrhoea.jpg/330px-Gram-stain_of_gonorrhoea.jpg 1.5x, /upwiki/wikipedia/commons/thumb/5/56/Gram-stain_of_gonorrhoea.jpg/440px-Gram-stain_of_gonorrhoea.jpg 2x" data-file-width="3754" data-file-height="2299" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Gram-stain_of_gonorrhoea.jpg" class="internal" title="Enlarge"></a></div>Micrograph of <a href="/enwiki/wiki/Gram-stain" class="mw-redirect" title="Gram-stain">Gram-stained</a> <a href="/enwiki/wiki/Pus" title="Pus">pus</a> showing <i><a href="/enwiki/wiki/Neisseria_gonorrhoeae" title="Neisseria gonorrhoeae">Neisseria gonorrhoeae</a></i> bacteria inside phagocytes and their relative sizes</div></div></div>
<p>Phagocytes can also kill microbes by oxygen-independent methods, but these are not as effective as the oxygen-dependent ones. There are four main types. The first uses electrically charged proteins that damage the bacterium's <a href="/enwiki/wiki/Cell_membrane" title="Cell membrane">membrane</a>. The second type uses lysozymes; these enzymes break down the bacterial <a href="/enwiki/wiki/Cell_wall" title="Cell wall">cell wall</a>. The third type uses <a href="/enwiki/wiki/Lactoferrin" title="Lactoferrin">lactoferrins</a>, which are present in neutrophil granules and remove essential iron from bacteria.<sup id="cite_ref-13" class="reference"><a href="#cite_note-13">[13]</a></sup> The fourth type uses <a href="/enwiki/wiki/Proteases" class="mw-redirect" title="Proteases">proteases</a> and <a href="/enwiki/wiki/Hydrolytic_enzymes" class="mw-redirect" title="Hydrolytic enzymes">hydrolytic enzymes</a>; these enzymes are used to digest the proteins of destroyed bacteria.<sup id="cite_ref-14" class="reference"><a href="#cite_note-14">[14]</a></sup>
</p>
<h3><span class="mw-headline" id="Extracellular">Extracellular</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=4" title="Edit section: Extracellular">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p><a href="/enwiki/wiki/Interferon-gamma" class="mw-redirect" title="Interferon-gamma">Interferon-gamma</a>—which was once called macrophage activating factor—stimulates macrophages to produce <a href="/enwiki/wiki/Nitric_oxide" title="Nitric oxide">nitric oxide</a>. The source of interferon-gamma can be <a href="/enwiki/wiki/CD4%2B_T_cells" class="mw-redirect" title="CD4+ T cells">CD4<sup>+</sup> T cells</a>, <a href="/enwiki/wiki/CD8%2B_T_cells" class="mw-redirect" title="CD8+ T cells">CD8<sup>+</sup> T cells</a>, <a href="/enwiki/wiki/NK_cell" class="mw-redirect" title="NK cell">natural killer cells</a>, <a href="/enwiki/wiki/B_cells" class="mw-redirect" title="B cells">B cells</a>, <a href="/enwiki/wiki/NKT_cell" class="mw-redirect" title="NKT cell">natural killer T cells</a>, monocytes, macrophages, or dendritic cells.<sup id="cite_ref-pmid14525967_15-0" class="reference"><a href="#cite_note-pmid14525967-15">[15]</a></sup> Nitric oxide is then released from the macrophage and, because of its toxicity, kills microbes near the macrophage.<sup id="cite_ref-USC_5-5" class="reference"><a href="#cite_note-USC-5">[5]</a></sup> Activated macrophages produce and secrete <a href="/enwiki/wiki/Tumor_necrosis_factors" class="mw-redirect" title="Tumor necrosis factors">tumor necrosis factor</a>. This <a href="/enwiki/wiki/Cytokine" title="Cytokine">cytokine</a>—a class of signaling molecule<sup id="cite_ref-16" class="reference"><a href="#cite_note-16">[16]</a></sup>—kills cancer cells and cells infected by viruses, and helps to activate the other cells of the immune system.<sup id="cite_ref-autogenerated2_17-0" class="reference"><a href="#cite_note-autogenerated2-17">[17]</a></sup>
</p><p>In some diseases, e.g., the rare <a href="/enwiki/wiki/Chronic_granulomatous_disease" title="Chronic granulomatous disease">chronic granulomatous disease</a>, the efficiency of phagocytes is impaired, and recurrent bacterial infections are a problem.<sup id="cite_ref-pmid18846805_18-0" class="reference"><a href="#cite_note-pmid18846805-18">[18]</a></sup> In this disease there is an abnormality affecting different elements of oxygen-dependent killing. Other rare congenital abnormalities, such as <a href="/enwiki/wiki/Ch%C3%A9diak%E2%80%93Higashi_syndrome" title="Chédiak–Higashi syndrome">Chédiak–Higashi syndrome</a>, are also associated with defective killing of ingested microbes.<sup id="cite_ref-pmid18043242_19-0" class="reference"><a href="#cite_note-pmid18043242-19">[19]</a></sup>
</p>
<h3><span class="mw-headline" id="Viruses">Viruses</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=5" title="Edit section: Viruses">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p><a href="/enwiki/wiki/Virus" title="Virus">Viruses</a> can reproduce only inside cells, and they gain entry by using many of the receptors involved in immunity. Once inside the cell, viruses use the cell's biological machinery to their own advantage, forcing the cell to make hundreds of identical copies of themselves. Although phagocytes and other components of the innate immune system can, to a limited extent, control viruses, once a virus is inside a cell the adaptive immune responses, particularly the lymphocytes, are more important for defense.<sup id="cite_ref-20" class="reference"><a href="#cite_note-20">[20]</a></sup> At the sites of viral infections, lymphocytes often vastly outnumber all the other cells of the immune system; this is common in viral <a href="/enwiki/wiki/Meningitis" title="Meningitis">meningitis</a>.<sup id="cite_ref-pmid17962876_21-0" class="reference"><a href="#cite_note-pmid17962876-21">[21]</a></sup> Virus-infected cells that have been killed by lymphocytes are cleared from the body by phagocytes.<sup id="cite_ref-22" class="reference"><a href="#cite_note-22">[22]</a></sup>
</p>
<h2><span class="mw-headline" id="Role_in_apoptosis">Role in apoptosis</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=6" title="Edit section: Role in apoptosis">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<style data-mw-deduplicate="TemplateStyles:r1033289096">.mw-parser-output .hatnote{font-style:italic}.mw-parser-output div.hatnote{padding-left:1.6em;margin-bottom:0.5em}.mw-parser-output .hatnote i{font-style:normal}.mw-parser-output .hatnote+link+.hatnote{margin-top:-0.5em}</style><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Apoptosis" title="Apoptosis">Apoptosis</a></div>
<div class="thumb tright"><div class="thumbinner" style="width:172px;"><a href="/enwiki/wiki/File:Apoptosis.png" class="image"><img alt="" src="/upwiki/wikipedia/commons/thumb/8/86/Apoptosis.png/170px-Apoptosis.png" decoding="async" width="170" height="332" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/8/86/Apoptosis.png/255px-Apoptosis.png 1.5x, /upwiki/wikipedia/commons/8/86/Apoptosis.png 2x" data-file-width="262" data-file-height="511" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Apoptosis.png" class="internal" title="Enlarge"></a></div>Apoptosis—phagocytes clear fragments of dead cells from the body</div></div></div>
<p>In an animal, cells are constantly dying. A balance between <a href="/enwiki/wiki/Cell_division" title="Cell division">cell division</a> and cell death keeps the number of cells relatively constant in adults.<sup id="cite_ref-pathogenesis_23-0" class="reference"><a href="#cite_note-pathogenesis-23">[23]</a></sup> There are two different ways a cell can die: by <a href="/enwiki/wiki/Necrosis" title="Necrosis">necrosis</a> or by apoptosis. In contrast to necrosis, which often results from disease or trauma, apoptosis—or <a href="/enwiki/wiki/Programmed_cell_death" title="Programmed cell death">programmed cell death</a>—is a normal healthy function of cells. The body has to rid itself of millions of dead or dying cells every day, and phagocytes play a crucial role in this process.<sup id="cite_ref-24" class="reference"><a href="#cite_note-24">[24]</a></sup>
</p><p>Dying cells that undergo the final stages of <a href="/enwiki/wiki/Apoptosis" title="Apoptosis">apoptosis</a><sup id="cite_ref-25" class="reference"><a href="#cite_note-25">[25]</a></sup> display molecules, such as <a href="/enwiki/wiki/Phosphatidylserine" title="Phosphatidylserine">phosphatidylserine</a>, on their cell surface to attract phagocytes.<sup id="cite_ref-pmid14645847_26-0" class="reference"><a href="#cite_note-pmid14645847-26">[26]</a></sup> Phosphatidylserine is normally found on the <a href="/enwiki/wiki/Cytoplasm" title="Cytoplasm">cytosolic</a> surface of the plasma membrane, but is redistributed during apoptosis to the extracellular surface by a protein known as <a href="/enwiki/wiki/Scramblase" class="mw-redirect" title="Scramblase">scramblase</a>.<sup id="cite_ref-pmid31837595_27-0" class="reference"><a href="#cite_note-pmid31837595-27">[27]</a></sup><sup id="cite_ref-phago2_28-0" class="reference"><a href="#cite_note-phago2-28">[28]</a></sup> These molecules mark the cell for phagocytosis by cells that possess the appropriate receptors, such as macrophages.<sup id="cite_ref-phago1_29-0" class="reference"><a href="#cite_note-phago1-29">[29]</a></sup> The removal of dying cells by phagocytes occurs in an orderly manner without eliciting an <a href="/enwiki/wiki/Inflammatory_response" class="mw-redirect" title="Inflammatory response">inflammatory response</a> and is an important function of phagocytes.<sup id="cite_ref-pmid18774293_30-0" class="reference"><a href="#cite_note-pmid18774293-30">[30]</a></sup>
</p>
<h2><span class="mw-headline" id="Interactions_with_other_cells">Interactions with other cells</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=7" title="Edit section: Interactions with other cells">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<p>Phagocytes are usually not bound to any particular <a href="/enwiki/wiki/Organ_(anatomy)" class="mw-redirect" title="Organ (anatomy)">organ</a> but move through the body interacting with the other phagocytic and non-phagocytic cells of the immune system. They can communicate with other cells by producing chemicals called <a href="/enwiki/wiki/Cytokines" class="mw-redirect" title="Cytokines">cytokines</a>, which recruit other phagocytes to the site of infections or stimulate dormant <a href="/enwiki/wiki/Lymphocyte" title="Lymphocyte">lymphocytes</a>.<sup id="cite_ref-31" class="reference"><a href="#cite_note-31">[31]</a></sup> Phagocytes form part of the <a href="/enwiki/wiki/Innate_immune_system" title="Innate immune system">innate immune system</a>, which animals, including humans, are born with. Innate immunity is very effective but non-specific in that it does not discriminate between different sorts of invaders. On the other hand, the <a href="/enwiki/wiki/Adaptive_immune_system" title="Adaptive immune system">adaptive immune system</a> of jawed vertebrates—the basis of acquired immunity—is highly specialized and can protect against almost any type of invader.<sup id="cite_ref-32" class="reference"><a href="#cite_note-32">[32]</a></sup> The adaptive immune system is not dependent on phagocytes but lymphocytes, which produce protective proteins called <a href="/enwiki/wiki/Antibody" title="Antibody">antibodies</a>, which tag invaders for destruction and prevent viruses from infecting cells.<sup id="cite_ref-33" class="reference"><a href="#cite_note-33">[33]</a></sup> Phagocytes, in particular dendritic cells and macrophages, stimulate lymphocytes to produce antibodies by an important process called <a href="/enwiki/wiki/Antigen" title="Antigen">antigen</a> presentation.<sup id="cite_ref-34" class="reference"><a href="#cite_note-34">[34]</a></sup>
</p>
<h3><span class="mw-headline" id="Antigen_presentation">Antigen presentation</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=8" title="Edit section: Antigen presentation">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Antigen_presentation" title="Antigen presentation">Antigen presentation</a></div>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:MHC_Class_I_processing.svg" class="image"><img alt="" src="/upwiki/wikipedia/commons/thumb/d/d7/MHC_Class_I_processing.svg/220px-MHC_Class_I_processing.svg.png" decoding="async" width="220" height="265" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/d/d7/MHC_Class_I_processing.svg/330px-MHC_Class_I_processing.svg.png 1.5x, /upwiki/wikipedia/commons/thumb/d/d7/MHC_Class_I_processing.svg/440px-MHC_Class_I_processing.svg.png 2x" data-file-width="493" data-file-height="594" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:MHC_Class_I_processing.svg" class="internal" title="Enlarge"></a></div>A schematic diagram of the presentation of foreign peptides by MHC 1 molecules</div></div></div>
<p>Antigen presentation is a process in which some phagocytes move parts of engulfed materials back to the surface of their cells and "present" them to other cells of the immune system.<sup id="cite_ref-35" class="reference"><a href="#cite_note-35">[35]</a></sup> There are two "professional" antigen-presenting cells: macrophages and dendritic cells.<sup id="cite_ref-paper_36-0" class="reference"><a href="#cite_note-paper-36">[36]</a></sup> After engulfment, foreign proteins (the <a href="/enwiki/wiki/Antigen" title="Antigen">antigens</a>) are broken down into <a href="/enwiki/wiki/Peptide" title="Peptide">peptides</a> inside dendritic cells and macrophages. These peptides are then bound to the cell's <a href="/enwiki/wiki/Major_histocompatibility_complex" title="Major histocompatibility complex">major histocompatibility complex</a> (MHC) glycoproteins, which carry the peptides back to the phagocyte's surface where they can be "presented" to lymphocytes.<sup id="cite_ref-ATP_37-0" class="reference"><a href="#cite_note-ATP-37">[37]</a></sup> Mature macrophages do not travel far from the site of infection, but dendritic cells can reach the body's <a href="/enwiki/wiki/Lymph_node" title="Lymph node">lymph nodes</a>, where there are millions of lymphocytes.<sup id="cite_ref-38" class="reference"><a href="#cite_note-38">[38]</a></sup> This enhances immunity because the lymphocytes respond to the antigens presented by the dendritic cells just as they would at the site of the original infection.<sup id="cite_ref-39" class="reference"><a href="#cite_note-39">[39]</a></sup> But dendritic cells can also destroy or pacify lymphocytes if they recognize components of the host body; this is necessary to prevent autoimmune reactions. This process is called tolerance.<sup id="cite_ref-40" class="reference"><a href="#cite_note-40">[40]</a></sup>
</p>
<h3><span class="mw-headline" id="Immunological_tolerance">Immunological tolerance</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=9" title="Edit section: Immunological tolerance">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Immunological_tolerance" class="mw-redirect" title="Immunological tolerance">Immunological tolerance</a></div>
<p>Dendritic cells also promote immunological tolerance,<sup id="cite_ref-somethingcool_41-0" class="reference"><a href="#cite_note-somethingcool-41">[41]</a></sup> which stops the body from attacking itself. The first type of tolerance is <a href="/enwiki/wiki/Central_tolerance" title="Central tolerance">central tolerance</a>, that occurs in the thymus. <a href="/enwiki/wiki/T_cell" title="T cell">T cells</a> that bind (via their T cell receptor) to self antigen (presented by dendritic cells on MHC molecules) too strongly are induced to die. The second type of immunological tolerance is <a href="/enwiki/wiki/Peripheral_tolerance" title="Peripheral tolerance">peripheral tolerance</a>.
Some self reactive T cells escape the thymus for a number of reasons, mainly due to the lack of expression of some self antigens in the thymus. Another type of T cell; T regulatory cells can down regulate self reactive T cells in the periphery.<sup id="cite_ref-rocky_42-0" class="reference"><a href="#cite_note-rocky-42">[42]</a></sup> When immunological tolerance fails, <a href="/enwiki/wiki/Autoimmune_disease" title="Autoimmune disease">autoimmune diseases</a> can follow.<sup id="cite_ref-43" class="reference"><a href="#cite_note-43">[43]</a></sup>
</p>
<h2><span class="mw-headline" id="Professional_phagocytes">Professional phagocytes</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=10" title="Edit section: Professional phagocytes">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Myeloid_cells.png" class="image"><img alt="A cartoon showing the relationships between a stem cell and mature white blood cells. Eight different types of white blood cell can derive from the same stem cell." src="/upwiki/wikipedia/commons/thumb/c/c0/Myeloid_cells.png/220px-Myeloid_cells.png" decoding="async" width="220" height="171" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/c/c0/Myeloid_cells.png/330px-Myeloid_cells.png 1.5x, /upwiki/wikipedia/commons/thumb/c/c0/Myeloid_cells.png/440px-Myeloid_cells.png 2x" data-file-width="864" data-file-height="671" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Myeloid_cells.png" class="internal" title="Enlarge"></a></div>Phagocytes derive from stem cells in the bone marrow</div></div></div>
<p>Phagocytes of humans and other jawed vertebrates are divided into "professional" and "non-professional" groups based on the efficiency with which they participate in phagocytosis.<sup id="cite_ref-Ernst186_44-0" class="reference"><a href="#cite_note-Ernst186-44">[44]</a></sup> The professional phagocytes are the <a href="/enwiki/wiki/Monocytes" class="mw-redirect" title="Monocytes">monocytes</a>, <a href="/enwiki/wiki/Macrophages" class="mw-redirect" title="Macrophages">macrophages</a>, <a href="/enwiki/wiki/Neutrophils" class="mw-redirect" title="Neutrophils">neutrophils</a>, tissue <a href="/enwiki/wiki/Dendritic_cell" title="Dendritic cell">dendritic cells</a> and <a href="/enwiki/wiki/Mast_cell" title="Mast cell">mast cells</a>.<sup id="cite_ref-Rob_45-0" class="reference"><a href="#cite_note-Rob-45">[45]</a></sup> One <a href="/enwiki/wiki/Litre" title="Litre">litre</a> of human blood contains about six billion phagocytes.<sup id="cite_ref-Hoff-values_46-0" class="reference"><a href="#cite_note-Hoff-values-46">[46]</a></sup>
</p>
<h3><span class="mw-headline" id="Activation">Activation</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=11" title="Edit section: Activation">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p>All phagocytes, and especially macrophages, exist in degrees of readiness. Macrophages are usually relatively dormant in the tissues and proliferate slowly. In this semi-resting state, they clear away dead host cells and other non-infectious debris and rarely take part in antigen presentation. But, during an infection, they receive chemical signals—usually <a href="/enwiki/wiki/Interferon_gamma" title="Interferon gamma">interferon gamma</a>—which increases their production of <a href="/enwiki/wiki/MHC_class_II" title="MHC class II">MHC II</a> molecules and which prepares them for presenting antigens. In this state, macrophages are good antigen presenters and killers. If they receive a signal directly from an invader, they become "hyperactivated", stop proliferating, and concentrate on killing. Their size and rate of phagocytosis increases—some become large enough to engulf invading <a href="/enwiki/wiki/Protozoa" title="Protozoa">protozoa</a>.<sup id="cite_ref-47" class="reference"><a href="#cite_note-47">[47]</a></sup>
</p><p>In the blood, neutrophils are inactive but are swept along at high speed. When they receive signals from macrophages at the sites of inflammation, they slow down and leave the blood. In the tissues, they are activated by cytokines and arrive at the battle scene ready to kill.<sup id="cite_ref-48" class="reference"><a href="#cite_note-48">[48]</a></sup>
</p>
<h3><span class="mw-headline" id="Migration">Migration</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=12" title="Edit section: Migration">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<div class="thumb tright"><div class="thumbinner" style="width:172px;"><a href="/enwiki/wiki/File:NeutrophilerAktion.svg" class="image"><img alt="A cartoon depicting a blood vessel and its surrounding tissue cells. There are three similar white blood cells, one in the blood and two among the tissue cells. The ones in the tissue are producing granules that can destroy bacteria." src="/upwiki/wikipedia/commons/thumb/e/e3/NeutrophilerAktion.svg/170px-NeutrophilerAktion.svg.png" decoding="async" width="170" height="215" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/e/e3/NeutrophilerAktion.svg/255px-NeutrophilerAktion.svg.png 1.5x, /upwiki/wikipedia/commons/thumb/e/e3/NeutrophilerAktion.svg/340px-NeutrophilerAktion.svg.png 2x" data-file-width="598" data-file-height="756" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:NeutrophilerAktion.svg" class="internal" title="Enlarge"></a></div>Neutrophils move from the blood to the site of infection</div></div></div>
<p>When an infection occurs, a chemical "SOS" signal is given off to attract phagocytes to the site.<sup id="cite_ref-49" class="reference"><a href="#cite_note-49">[49]</a></sup> These chemical signals may include proteins from invading bacteria, clotting system <a href="/enwiki/wiki/Peptides" class="mw-redirect" title="Peptides">peptides</a>, <a href="/enwiki/wiki/Complement_system" title="Complement system">complement</a> products, and cytokines that have been given off by macrophages located in the tissue near the infection site.<sup id="cite_ref-USC_5-6" class="reference"><a href="#cite_note-USC-5">[5]</a></sup> Another group of chemical attractants are <a href="/enwiki/wiki/Cytokines" class="mw-redirect" title="Cytokines">cytokines</a> that recruit neutrophils and monocytes from the blood.<sup id="cite_ref-money_50-0" class="reference"><a href="#cite_note-money-50">[50]</a></sup>
</p><p>To reach the site of infection, phagocytes leave the bloodstream and enter the affected tissues. Signals from the infection cause the <a href="/enwiki/wiki/Endothelial" class="mw-redirect" title="Endothelial">endothelial</a> cells that line the blood vessels to make a protein called <a href="/enwiki/wiki/Selectin" title="Selectin">selectin</a>, which neutrophils stick to on passing by. Other signals called <a href="/enwiki/wiki/Vasodilator" class="mw-redirect" title="Vasodilator">vasodilators</a> loosen the junctions connecting endothelial cells, allowing the phagocytes to pass through the wall. <a href="/enwiki/wiki/Chemotaxis" title="Chemotaxis">Chemotaxis</a> is the process by which phagocytes follow the cytokine "scent" to the infected spot.<sup id="cite_ref-USC_5-7" class="reference"><a href="#cite_note-USC-5">[5]</a></sup> Neutrophils travel across <a href="/enwiki/wiki/Epithelial" class="mw-redirect" title="Epithelial">epithelial</a> cell-lined organs to sites of infection, and although this is an important component of fighting infection, the migration itself can result in disease-like symptoms.<sup id="cite_ref-pmid14519390_51-0" class="reference"><a href="#cite_note-pmid14519390-51">[51]</a></sup> During an infection, millions of neutrophils are recruited from the blood, but they die after a few days.<sup id="cite_ref-52" class="reference"><a href="#cite_note-52">[52]</a></sup>
</p>
<h3><span class="mw-headline" id="Monocytes">Monocytes</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=13" title="Edit section: Monocytes">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Monocytes" class="mw-redirect" title="Monocytes">Monocytes</a></div>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Monocytes,_a_type_of_white_blood_cell_(Giemsa_stained).jpg" class="image"><img alt="" src="/upwiki/wikipedia/commons/thumb/e/e6/Monocytes%2C_a_type_of_white_blood_cell_%28Giemsa_stained%29.jpg/220px-Monocytes%2C_a_type_of_white_blood_cell_%28Giemsa_stained%29.jpg" decoding="async" width="220" height="160" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/e/e6/Monocytes%2C_a_type_of_white_blood_cell_%28Giemsa_stained%29.jpg/330px-Monocytes%2C_a_type_of_white_blood_cell_%28Giemsa_stained%29.jpg 1.5x, /upwiki/wikipedia/commons/thumb/e/e6/Monocytes%2C_a_type_of_white_blood_cell_%28Giemsa_stained%29.jpg/440px-Monocytes%2C_a_type_of_white_blood_cell_%28Giemsa_stained%29.jpg 2x" data-file-width="1455" data-file-height="1060" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Monocytes,_a_type_of_white_blood_cell_(Giemsa_stained).jpg" class="internal" title="Enlarge"></a></div>Monocytes in blood (<a href="/enwiki/wiki/Giemsa_stain" title="Giemsa stain">Giemsa stain</a>)</div></div></div>
<p>Monocytes develop in the bone marrow and reach maturity in the blood. Mature monocytes have large, smooth, lobed nuclei and abundant <a href="/enwiki/wiki/Cytoplasm" title="Cytoplasm">cytoplasm</a> that contains granules. Monocytes ingest foreign or dangerous substances and present <a href="/enwiki/wiki/Antigens" class="mw-redirect" title="Antigens">antigens</a> to other cells of the immune system. Monocytes form two groups: a circulating group and a marginal group that remain in other tissues (approximately 70% are in the marginal group). Most monocytes leave the blood stream after 20–40 hours to travel to tissues and organs and in doing so transform into macrophages<sup id="cite_ref-53" class="reference"><a href="#cite_note-53">[53]</a></sup> or dendritic cells depending on the signals they receive.<sup id="cite_ref-54" class="reference"><a href="#cite_note-54">[54]</a></sup> There are about 500 million monocytes in one litre of human blood.<sup id="cite_ref-Hoff-values_46-1" class="reference"><a href="#cite_note-Hoff-values-46">[46]</a></sup>
</p>
<h3><span class="mw-headline" id="Macrophages">Macrophages</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=14" title="Edit section: Macrophages">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Macrophages" class="mw-redirect" title="Macrophages">Macrophages</a></div>
<p>Mature macrophages do not travel far but stand guard over those areas of the body that are exposed to the outside world. There they act as garbage collectors, antigen presenting cells, or ferocious killers, depending on the signals they receive.<sup id="cite_ref-55" class="reference"><a href="#cite_note-55">[55]</a></sup> They derive from monocytes, <a href="/enwiki/wiki/Granulocyte" title="Granulocyte">granulocyte</a> stem cells, or the <a href="/enwiki/wiki/Cell_division" title="Cell division">cell division</a> of pre-existing macrophages.<sup id="cite_ref-pmid8870002_56-0" class="reference"><a href="#cite_note-pmid8870002-56">[56]</a></sup> Human macrophages are about 21 <a href="/enwiki/wiki/Micrometre" title="Micrometre">micrometers</a> in diameter.<sup id="cite_ref-57" class="reference"><a href="#cite_note-57">[57]</a></sup>
</p>
<div class="thumb tleft"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg" class="image"><img alt="A person's thigh with a red area that is inflamed. At the centre of the inflammation is a wound with pus." src="/upwiki/wikipedia/commons/thumb/3/3b/Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg/220px-Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg" decoding="async" width="220" height="145" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/3/3b/Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg/330px-Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg 1.5x, /upwiki/wikipedia/commons/thumb/3/3b/Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg/440px-Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg 2x" data-file-width="2800" data-file-height="1850" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Cutaneous_abscess_MRSA_staphylococcus_aureus_7826_lores.jpg" class="internal" title="Enlarge"></a></div><a href="/enwiki/wiki/Pus" title="Pus">Pus</a> oozing from an <a href="/enwiki/wiki/Abscess" title="Abscess">abscess</a> caused by bacteria—pus contains millions of phagocytes</div></div></div>
<p>This type of phagocyte does not have granules but contains many <a href="/enwiki/wiki/Lysosome" title="Lysosome">lysosomes</a>. Macrophages are found throughout the body in almost all tissues and organs (e.g., <a href="/enwiki/wiki/Microglial_cell" class="mw-redirect" title="Microglial cell">microglial cells</a> in the <a href="/enwiki/wiki/Brain" title="Brain">brain</a> and <a href="/enwiki/wiki/Pulmonary_alveolus" title="Pulmonary alveolus">alveolar</a> macrophages in the <a href="/enwiki/wiki/Lungs" class="mw-redirect" title="Lungs">lungs</a>), where they silently lie in wait. A macrophage's location can determine its size and appearance. Macrophages cause inflammation through the production of <a href="/enwiki/wiki/Interleukin-1" class="mw-redirect" title="Interleukin-1">interleukin-1</a>, <a href="/enwiki/wiki/Interleukin-6" class="mw-redirect" title="Interleukin-6">interleukin-6</a>, and <a href="/enwiki/wiki/Tumor_necrosis_factor-alpha" class="mw-redirect" title="Tumor necrosis factor-alpha">TNF-alpha</a>.<sup id="cite_ref-USCmac_58-0" class="reference"><a href="#cite_note-USCmac-58">[58]</a></sup> Macrophages are usually only found in tissue and are rarely seen in blood circulation. The life-span of tissue macrophages has been estimated to range from four to fifteen days.<sup id="cite_ref-59" class="reference"><a href="#cite_note-59">[59]</a></sup>
</p><p>Macrophages can be activated to perform functions that a resting monocyte cannot.<sup id="cite_ref-USCmac_58-1" class="reference"><a href="#cite_note-USCmac-58">[58]</a></sup> <a href="/enwiki/wiki/T_helper_cell" title="T helper cell">T helper cells</a> (also known as effector T cells or T<sub>h</sub> cells), a sub-group of lymphocytes, are responsible for the activation of macrophages. T<sub>h</sub>1 cells activate macrophages by signaling with <a href="/enwiki/wiki/IFN-gamma" class="mw-redirect" title="IFN-gamma">IFN-gamma</a> and displaying the protein <a href="/enwiki/wiki/CD40_ligand" class="mw-redirect" title="CD40 ligand">CD40 ligand</a>.<sup id="cite_ref-60" class="reference"><a href="#cite_note-60">[60]</a></sup> Other signals include TNF-alpha and <a href="/enwiki/wiki/Lipopolysaccharides" class="mw-redirect" title="Lipopolysaccharides">lipopolysaccharides</a> from bacteria.<sup id="cite_ref-USCmac_58-2" class="reference"><a href="#cite_note-USCmac-58">[58]</a></sup> T<sub>h</sub>1 cells can recruit other phagocytes to the site of the infection in several ways. They secrete cytokines that act on the <a href="/enwiki/wiki/Bone_marrow" title="Bone marrow">bone marrow</a> to stimulate the production of monocytes and neutrophils, and they secrete some of the <a href="/enwiki/wiki/Cytokine" title="Cytokine">cytokines</a> that are responsible for the migration of monocytes and neutrophils out of the bloodstream.<sup id="cite_ref-61" class="reference"><a href="#cite_note-61">[61]</a></sup> T<sub>h</sub>1 cells come from the <a href="/enwiki/wiki/Cellular_differentiation" title="Cellular differentiation">differentiation</a> of CD4<sup>+</sup> T cells once they have responded to antigen in the <a href="/enwiki/wiki/Lymphatic_system" title="Lymphatic system">secondary lymphoid tissues</a>.<sup id="cite_ref-USCmac_58-3" class="reference"><a href="#cite_note-USCmac-58">[58]</a></sup> Activated macrophages play a potent role in <a href="/enwiki/wiki/Tumor" class="mw-redirect" title="Tumor">tumor</a> destruction by producing TNF-alpha, IFN-gamma, nitric oxide, reactive oxygen compounds, <a href="/enwiki/wiki/Cation" class="mw-redirect" title="Cation">cationic</a> proteins, and hydrolytic enzymes.<sup id="cite_ref-USCmac_58-4" class="reference"><a href="#cite_note-USCmac-58">[58]</a></sup>
</p>
<h3><span class="mw-headline" id="Neutrophils">Neutrophils</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=15" title="Edit section: Neutrophils">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Neutrophils" class="mw-redirect" title="Neutrophils">Neutrophils</a></div>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Neutrophils.jpg" class="image"><img alt="A round cell with a lobed nucleus surrounded by many slightly smaller red blood cells." src="/upwiki/wikipedia/commons/thumb/0/09/Neutrophils.jpg/220px-Neutrophils.jpg" decoding="async" width="220" height="160" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/0/09/Neutrophils.jpg/330px-Neutrophils.jpg 1.5x, /upwiki/wikipedia/commons/thumb/0/09/Neutrophils.jpg/440px-Neutrophils.jpg 2x" data-file-width="1455" data-file-height="1060" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Neutrophils.jpg" class="internal" title="Enlarge"></a></div>Neutrophils with a segmented nuclei surrounded by <a href="/enwiki/wiki/Erythrocytes" class="mw-redirect" title="Erythrocytes">erythrocytes</a>, the intra-cellular granules are visible in the <a href="/enwiki/wiki/Cytoplasm" title="Cytoplasm">cytoplasm</a> (<a href="/enwiki/wiki/Giemsa_stain" title="Giemsa stain">Giemsa stained</a>)</div></div></div>
<p>Neutrophils are normally found in the <a href="/enwiki/wiki/Circulatory_system" title="Circulatory system">bloodstream</a> and are the most abundant type of phagocyte, constituting 50% to 60% of the total circulating white blood cells.<sup id="cite_ref-IandF_62-0" class="reference"><a href="#cite_note-IandF-62">[62]</a></sup> One litre of human blood contains about five billion neutrophils,<sup id="cite_ref-Hoff-values_46-2" class="reference"><a href="#cite_note-Hoff-values-46">[46]</a></sup> which are about 10 micrometers in diameter<sup id="cite_ref-63" class="reference"><a href="#cite_note-63">[63]</a></sup> and live for only about five days.<sup id="cite_ref-autogenerated2_17-1" class="reference"><a href="#cite_note-autogenerated2-17">[17]</a></sup> Once they have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection.<sup id="cite_ref-Som18_64-0" class="reference"><a href="#cite_note-Som18-64">[64]</a></sup> They are ferocious eaters and rapidly engulf invaders coated with <a href="/enwiki/wiki/Antibody" title="Antibody">antibodies</a> and <a href="/enwiki/wiki/Complement_system" title="Complement system">complement</a>, and damaged cells or cellular debris. Neutrophils do not return to the blood; they turn into <a href="/enwiki/wiki/Pus" title="Pus">pus</a> cells and die.<sup id="cite_ref-Som18_64-1" class="reference"><a href="#cite_note-Som18-64">[64]</a></sup> Mature neutrophils are smaller than monocytes and have a segmented <a href="/enwiki/wiki/Cell_nucleus" title="Cell nucleus">nucleus</a> with several sections; each section is connected by <a href="/enwiki/wiki/Chromatin" title="Chromatin">chromatin</a> filaments—neutrophils can have 2–5 segments. Neutrophils do not normally exit the bone marrow until maturity but during an infection neutrophil precursors called <a href="/enwiki/wiki/Metamyelocyte" title="Metamyelocyte">metamyelocytes</a>, <a href="/enwiki/wiki/Myelocyte" title="Myelocyte">myelocytes</a> and <a href="/enwiki/wiki/Promyelocyte" title="Promyelocyte">promyelocytes</a> are released.<sup id="cite_ref-pmid9853933_65-0" class="reference"><a href="#cite_note-pmid9853933-65">[65]</a></sup>
</p><p>The intra-cellular granules of the human neutrophil have long been recognized for their protein-destroying and bactericidal properties.<sup id="cite_ref-66" class="reference"><a href="#cite_note-66">[66]</a></sup> Neutrophils can secrete products that stimulate monocytes and macrophages. Neutrophil secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing.<sup id="cite_ref-pmid17991288_67-0" class="reference"><a href="#cite_note-pmid17991288-67">[67]</a></sup> Secretions from the <a href="/enwiki/wiki/Azurophilic_granules" class="mw-redirect" title="Azurophilic granules">primary granules</a> of neutrophils stimulate the phagocytosis of <a href="/enwiki/wiki/IgG" class="mw-redirect" title="IgG">IgG</a>-antibody-coated bacteria.<sup id="cite_ref-pmid18787642_68-0" class="reference"><a href="#cite_note-pmid18787642-68">[68]</a></sup> When encountering bacteria, fungi or activated platelets they produce web-like chromatin structures known as <a href="/enwiki/wiki/Neutrophil_extracellular_traps" title="Neutrophil extracellular traps">neutrophil extracellular traps</a> (NETs). Composed mainly of DNA, NETs cause death by a process called netosis – after the pathogens are trapped in NETs they are killed by oxidative and non-oxidative mechanisms.<sup id="cite_ref-pmid28990587_69-0" class="reference"><a href="#cite_note-pmid28990587-69">[69]</a></sup>
</p>
<h3><span class="mw-headline" id="Dendritic_cells">Dendritic cells</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=16" title="Edit section: Dendritic cells">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Dendritic_cell" title="Dendritic cell">Dendritic cell</a></div>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Dendritic_cell.JPG" class="image"><img alt="One dendritic cell, which is almost the shape of a star. Its edges are ragged." src="/upwiki/wikipedia/commons/thumb/3/3b/Dendritic_cell.JPG/220px-Dendritic_cell.JPG" decoding="async" width="220" height="183" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/3/3b/Dendritic_cell.JPG/330px-Dendritic_cell.JPG 1.5x, /upwiki/wikipedia/commons/thumb/3/3b/Dendritic_cell.JPG/440px-Dendritic_cell.JPG 2x" data-file-width="580" data-file-height="483" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Dendritic_cell.JPG" class="internal" title="Enlarge"></a></div>A dendritic cell</div></div></div>
<p>Dendritic cells are specialized antigen-presenting cells that have long outgrowths called dendrites,<sup id="cite_ref-Steinman_70-0" class="reference"><a href="#cite_note-Steinman-70">[70]</a></sup> that help to engulf microbes and other invaders.<sup id="cite_ref-rock_71-0" class="reference"><a href="#cite_note-rock-71">[71]</a></sup><sup id="cite_ref-antigen_72-0" class="reference"><a href="#cite_note-antigen-72">[72]</a></sup> Dendritic cells are present in the tissues that are in contact with the external environment, mainly the skin, the inner lining of the nose, the lungs, the stomach, and the intestines.<sup id="cite_ref-73" class="reference"><a href="#cite_note-73">[73]</a></sup> Once activated, they mature and migrate to the lymphoid tissues where they interact with <a href="/enwiki/wiki/T_cells" class="mw-redirect" title="T cells">T cells</a> and <a href="/enwiki/wiki/B_cells" class="mw-redirect" title="B cells">B cells</a> to initiate and orchestrate the adaptive immune response.<sup id="cite_ref-74" class="reference"><a href="#cite_note-74">[74]</a></sup>
Mature dendritic cells activate <a href="/enwiki/wiki/T_helper_cell" title="T helper cell">T helper cells</a> and <a href="/enwiki/wiki/Cytotoxic_T_cell" title="Cytotoxic T cell">cytotoxic T cells</a>.<sup id="cite_ref-75" class="reference"><a href="#cite_note-75">[75]</a></sup> The activated helper T cells interact with macrophages and B cells to activate them in turn. In addition, dendritic cells can influence the type of immune response produced; when they travel to the lymphoid areas where T cells are held they can activate T cells, which then differentiate into cytotoxic T cells or helper T cells.<sup id="cite_ref-rock_71-1" class="reference"><a href="#cite_note-rock-71">[71]</a></sup>
</p>
<h3><span class="mw-headline" id="Mast_cells">Mast cells</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=17" title="Edit section: Mast cells">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1033289096"/><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/enwiki/wiki/Mast_cell" title="Mast cell">Mast cell</a></div>
<p>Mast cells have <a href="/enwiki/wiki/Toll-like_receptor" title="Toll-like receptor">Toll-like receptors</a> and interact with dendritic cells, B cells, and T cells to help mediate adaptive immune functions.<sup id="cite_ref-pmid19672091_76-0" class="reference"><a href="#cite_note-pmid19672091-76">[76]</a></sup> Mast cells express <a href="/enwiki/wiki/MHC_class_II" title="MHC class II">MHC class II</a> molecules and can participate in antigen presentation; however, the mast cell's role in antigen presentation is not very well understood.<sup id="cite_ref-pmid18936782_77-0" class="reference"><a href="#cite_note-pmid18936782-77">[77]</a></sup> Mast cells can consume and kill <a href="/enwiki/wiki/Gram-negative_bacteria" title="Gram-negative bacteria">gram-negative bacteria</a> (e.g., <a href="/enwiki/wiki/Salmonella" title="Salmonella">salmonella</a>), and process their antigens.<sup id="cite_ref-mast_78-0" class="reference"><a href="#cite_note-mast-78">[78]</a></sup> They specialize in processing the <a href="/enwiki/wiki/Fimbria_(bacteriology)" class="mw-redirect" title="Fimbria (bacteriology)">fimbrial proteins</a> on the surface of bacteria, which are involved in adhesion to tissues.<sup id="cite_ref-pmid8790416_79-0" class="reference"><a href="#cite_note-pmid8790416-79">[79]</a></sup><sup id="cite_ref-pmid8568252_80-0" class="reference"><a href="#cite_note-pmid8568252-80">[80]</a></sup> In addition to these functions, mast cells produce cytokines that induce an inflammatory response.<sup id="cite_ref-pmid11424870_81-0" class="reference"><a href="#cite_note-pmid11424870-81">[81]</a></sup> This is a vital part of the destruction of microbes because the cytokines attract more phagocytes to the site of infection.<sup id="cite_ref-mast_78-1" class="reference"><a href="#cite_note-mast-78">[78]</a></sup><sup id="cite_ref-pmid22577358_82-0" class="reference"><a href="#cite_note-pmid22577358-82">[82]</a></sup>
</p>
<table class="wikitable" style="margin:1em auto 1em auto;">
<caption><b>Professional Phagocytes</b><sup id="cite_ref-superman_83-0" class="reference"><a href="#cite_note-superman-83">[83]</a></sup>
</caption>
<tbody><tr>
<th>Main location
</th>
<th>Variety of <a href="/enwiki/wiki/Phenotype" title="Phenotype">phenotypes</a>
</th></tr>
<tr>
<td>Blood
</td>
<td>neutrophils, monocytes
</td></tr>
<tr>
<td>Bone marrow
</td>
<td>macrophages, monocytes, <a href="/enwiki/wiki/Sinusoid_(blood_vessel)" class="mw-redirect" title="Sinusoid (blood vessel)">sinusoidal cells</a>, <a href="/enwiki/wiki/List_of_distinct_cell_types_in_the_adult_human_body#Epithelial_cells_lining_closed_internal_body_cavities" title="List of distinct cell types in the adult human body">lining cells</a>
</td></tr>
<tr>
<td>Bone tissue
</td>
<td><a href="/enwiki/wiki/Osteoclast" title="Osteoclast">osteoclasts</a>
</td></tr>
<tr>
<td>Gut and intestinal <a href="/enwiki/wiki/Peyer%27s_patches" class="mw-redirect" title="Peyer's patches">Peyer's patches</a>
</td>
<td>macrophages
</td></tr>
<tr>
<td><a href="/enwiki/wiki/Connective_tissue" title="Connective tissue">Connective tissue</a>
</td>
<td><a href="/enwiki/wiki/Histiocyte" title="Histiocyte">histiocytes</a>, macrophages, monocytes, dendritic cells
</td></tr>
<tr>
<td>Liver
</td>
<td><a href="/enwiki/wiki/Kupffer_cell" title="Kupffer cell">Kupffer cells</a>, monocytes
</td></tr>
<tr>
<td>Lung
</td>
<td>self-replicating macrophages, monocytes, mast cells, dendritic cells
</td></tr>
<tr>
<td><a href="/enwiki/wiki/Lymphatic_system" title="Lymphatic system">Lymphoid tissue</a>
</td>
<td>free and fixed macrophages and monocytes, dendritic cells
</td></tr>
<tr>
<td>Nervous tissue
</td>
<td><a href="/enwiki/wiki/Microglial_cell" class="mw-redirect" title="Microglial cell">microglial cells</a> (<a href="/enwiki/wiki/CD4" title="CD4">CD4</a><sup>+</sup>)
</td></tr>
<tr>
<td><a href="/enwiki/wiki/Spleen" title="Spleen">Spleen</a>
</td>
<td>free and fixed macrophages, monocytes, sinusoidal cells
</td></tr>
<tr>
<td><a href="/enwiki/wiki/Thymus" title="Thymus">Thymus</a>
</td>
<td>free and fixed macrophages and monocytes
</td></tr>
<tr>
<td>Skin
</td>
<td>resident <a href="/enwiki/wiki/Langerhans_cell" title="Langerhans cell">Langerhans cells</a>, other dendritic cells, conventional macrophages, mast cells
</td></tr></tbody></table>
<h2><span class="mw-headline" id="Non-professional_phagocytes">Non-professional phagocytes</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=18" title="Edit section: Non-professional phagocytes">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<p>Dying cells and foreign organisms are consumed by cells other than the "professional" phagocytes.<sup id="cite_ref-pmid18451871_84-0" class="reference"><a href="#cite_note-pmid18451871-84">[84]</a></sup> These cells include <a href="/enwiki/wiki/Epithelial_cell" class="mw-redirect" title="Epithelial cell">epithelial cells</a>, <a href="/enwiki/wiki/Endothelial_cell" class="mw-redirect" title="Endothelial cell">endothelial cells</a>, <a href="/enwiki/wiki/Fibroblast" title="Fibroblast">fibroblasts</a>, and mesenchymal cells. They are called non-professional phagocytes, to emphasize that, in contrast to professional phagocytes, phagocytosis is not their principal function.<sup id="cite_ref-pmid11083817_85-0" class="reference"><a href="#cite_note-pmid11083817-85">[85]</a></sup> Fibroblasts, for example, which can phagocytose collagen in the process of remolding scars, will also make some attempt to ingest foreign particles.<sup id="cite_ref-86" class="reference"><a href="#cite_note-86">[86]</a></sup>
</p><p>Non-professional phagocytes are more limited than professional phagocytes in the type of particles they can take up. This is due to their lack of efficient phagocytic receptors, in particular <a href="/enwiki/wiki/Opsonin" title="Opsonin">opsonins</a>—which are antibodies and complement attached to invaders by the immune system.<sup id="cite_ref-something_87-0" class="reference"><a href="#cite_note-something-87">[87]</a></sup> Additionally, most non-professional phagocytes do not produce reactive oxygen-containing molecules in response to phagocytosis.<sup id="cite_ref-pmid14732160_88-0" class="reference"><a href="#cite_note-pmid14732160-88">[88]</a></sup>
</p>
<table class="wikitable" style="margin:1em auto 1em auto;">
<caption><b>Non-professional phagocytes</b><sup id="cite_ref-superman_83-1" class="reference"><a href="#cite_note-superman-83">[83]</a></sup>
</caption>
<tbody><tr>
<th>Main location
</th>
<th>Variety of phenotypes
</th></tr>
<tr>
<td>Blood, lymph and lymph nodes
</td>
<td>Lymphocytes
</td></tr>
<tr>
<td>Blood, lymph and lymph nodes
</td>
<td><a href="/enwiki/wiki/Natural_killer_cells" class="mw-redirect" title="Natural killer cells">NK</a> and LGL cells (large granular lymphocytes)
</td></tr>
<tr>
<td>Blood
</td>
<td><a href="/enwiki/wiki/Eosinophils" class="mw-redirect" title="Eosinophils">Eosinophils</a> and <a href="/enwiki/wiki/Basophils" class="mw-redirect" title="Basophils">Basophils</a><sup id="cite_ref-pmid29321780_89-0" class="reference"><a href="#cite_note-pmid29321780-89">[89]</a></sup>
</td></tr>
<tr>
<td>Skin
</td>
<td><a href="/enwiki/wiki/Epithelial_cell" class="mw-redirect" title="Epithelial cell">Epithelial cells</a>
</td></tr>
<tr>
<td>Blood vessels
</td>
<td><a href="/enwiki/wiki/Endothelial_cell" class="mw-redirect" title="Endothelial cell">Endothelial cells</a>
</td></tr>
<tr>
<td>Connective tissue
</td>
<td>Fibroblasts
</td></tr></tbody></table>
<h2><span class="mw-headline" id="Pathogen_evasion_and_resistance">Pathogen evasion and resistance</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=19" title="Edit section: Pathogen evasion and resistance">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<div class="thumb tright"><div class="thumbinner" style="width:172px;"><a href="/enwiki/wiki/File:Staphylococcus_aureus,_50,000x,_USDA,_ARS,_EMU.jpg" class="image"><img alt="Two round bacteria that are close together and are almost completely covered in a string-like substance." src="/upwiki/wikipedia/commons/thumb/6/68/Staphylococcus_aureus%2C_50%2C000x%2C_USDA%2C_ARS%2C_EMU.jpg/170px-Staphylococcus_aureus%2C_50%2C000x%2C_USDA%2C_ARS%2C_EMU.jpg" decoding="async" width="170" height="215" class="thumbimage" srcset="/upwiki/wikipedia/commons/thumb/6/68/Staphylococcus_aureus%2C_50%2C000x%2C_USDA%2C_ARS%2C_EMU.jpg/255px-Staphylococcus_aureus%2C_50%2C000x%2C_USDA%2C_ARS%2C_EMU.jpg 1.5x, /upwiki/wikipedia/commons/thumb/6/68/Staphylococcus_aureus%2C_50%2C000x%2C_USDA%2C_ARS%2C_EMU.jpg/340px-Staphylococcus_aureus%2C_50%2C000x%2C_USDA%2C_ARS%2C_EMU.jpg 2x" data-file-width="1184" data-file-height="1500" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Staphylococcus_aureus,_50,000x,_USDA,_ARS,_EMU.jpg" class="internal" title="Enlarge"></a></div>Cells of <i>Staphylococcus aureus</i> bacteria: the large, stringy capsules protect the organisms from attack by phagocytes.</div></div></div>
<p>A pathogen is only successful in infecting an organism if it can get past its defenses. Pathogenic bacteria and protozoa have developed a variety of methods to resist attacks by phagocytes, and many actually survive and replicate within phagocytic cells.<sup id="cite_ref-chicken_90-0" class="reference"><a href="#cite_note-chicken-90">[90]</a></sup><sup id="cite_ref-91" class="reference"><a href="#cite_note-91">[91]</a></sup>
</p>
<h3><span class="mw-headline" id="Avoiding_contact">Avoiding contact</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=20" title="Edit section: Avoiding contact">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p>There are several ways bacteria avoid contact with phagocytes. First, they can grow in sites that phagocytes are not capable of traveling to (e.g., the surface of unbroken skin). Second, bacteria can suppress the <a href="/enwiki/wiki/Inflammatory_response" class="mw-redirect" title="Inflammatory response">inflammatory response</a>; without this response to infection phagocytes cannot respond adequately. Third, some species of bacteria can inhibit the ability of phagocytes to travel to the site of infection by interfering with chemotaxis.<sup id="cite_ref-chicken_90-1" class="reference"><a href="#cite_note-chicken-90">[90]</a></sup> Fourth, some bacteria can avoid contact with phagocytes by tricking the immune system into "thinking" that the bacteria are "self". <i><a href="/enwiki/wiki/Treponema_pallidum" title="Treponema pallidum">Treponema pallidum</a></i>—the bacterium that causes <a href="/enwiki/wiki/Syphilis" title="Syphilis">syphilis</a>—hides from phagocytes by coating its surface with <a href="/enwiki/wiki/Fibronectin" title="Fibronectin">fibronectin</a>,<sup id="cite_ref-pmid11973157_92-0" class="reference"><a href="#cite_note-pmid11973157-92">[92]</a></sup> which is produced naturally by the body and plays a crucial role in <a href="/enwiki/wiki/Wound_healing" title="Wound healing">wound healing</a>.<sup id="cite_ref-pmid15992798_93-0" class="reference"><a href="#cite_note-pmid15992798-93">[93]</a></sup>
</p>
<h3><span class="mw-headline" id="Avoiding_engulfment">Avoiding engulfment</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=21" title="Edit section: Avoiding engulfment">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p>Bacteria often produce <a href="/enwiki/wiki/Bacterial_capsule" title="Bacterial capsule">capsules</a> made of proteins or sugars that coat their cells and interfere with phagocytosis.<sup id="cite_ref-chicken_90-2" class="reference"><a href="#cite_note-chicken-90">[90]</a></sup> Some examples are the K5 capsule and O75 <a href="/enwiki/wiki/O_antigen" class="mw-redirect" title="O antigen">O antigen</a> found on the surface of <i><a href="/enwiki/wiki/Escherichia_coli" title="Escherichia coli">Escherichia coli</a></i>,<sup id="cite_ref-pmid10417134_94-0" class="reference"><a href="#cite_note-pmid10417134-94">[94]</a></sup> and the <a href="/enwiki/wiki/Exopolysaccharide" class="mw-redirect" title="Exopolysaccharide">exopolysaccharide</a> capsules of <i><a href="/enwiki/wiki/Staphylococcus_epidermidis" title="Staphylococcus epidermidis">Staphylococcus epidermidis</a></i>.<sup id="cite_ref-pmid15501828_95-0" class="reference"><a href="#cite_note-pmid15501828-95">[95]</a></sup> <i><a href="/enwiki/wiki/Streptococcus_pneumoniae" title="Streptococcus pneumoniae">Streptococcus pneumoniae</a></i> produces several types of capsule that provide different levels of protection,<sup id="cite_ref-pmid19047408_96-0" class="reference"><a href="#cite_note-pmid19047408-96">[96]</a></sup> and <a href="/enwiki/wiki/Group_A_streptococci" class="mw-redirect" title="Group A streptococci">group A streptococci</a> produce proteins such as <a href="/enwiki/wiki/M_protein_(Streptococcus)" title="M protein (Streptococcus)">M protein</a> and <a href="/enwiki/wiki/Fimbria_(bacteriology)" class="mw-redirect" title="Fimbria (bacteriology)">fimbrial proteins</a> to block engulfment. Some proteins hinder opsonin-related ingestion; <i><a href="/enwiki/wiki/Staphylococcus_aureus" title="Staphylococcus aureus">Staphylococcus aureus</a></i> produces <a href="/enwiki/wiki/Protein_A" title="Protein A">Protein A</a> to block antibody receptors, which decreases the effectiveness of opsonins.<sup id="cite_ref-pmid16322743_97-0" class="reference"><a href="#cite_note-pmid16322743-97">[97]</a></sup> Enteropathogenic species of the genus <a href="/enwiki/wiki/Yersinia" title="Yersinia">Yersinia</a> bind with the use of the virulence factor <a href="/enwiki/w/index.php?title=YopH&action=edit&redlink=1" class="new" title="YopH (page does not exist)">YopH</a> to receptors of phagocytes from which they influence the cells capability to exert phagocytosis.<sup id="cite_ref-pmid11890550_98-0" class="reference"><a href="#cite_note-pmid11890550-98">[98]</a></sup>
</p>
<h3><span class="mw-headline" id="Survival_inside_the_phagocyte">Survival inside the phagocyte</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=22" title="Edit section: Survival inside the phagocyte">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<div class="thumb tright"><div class="thumbinner" style="width:222px;"><a href="/enwiki/wiki/File:Rickettsia_rickettsii.jpg" class="image"><img alt="Two round cells with many tiny rod-shaped bacteria inside." src="/upwiki/wikipedia/commons/thumb/8/86/Rickettsia_rickettsii.jpg/220px-Rickettsia_rickettsii.jpg" decoding="async" width="220" height="206" class="thumbimage" srcset="/upwiki/wikipedia/commons/8/86/Rickettsia_rickettsii.jpg 1.5x" data-file-width="297" data-file-height="278" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Rickettsia_rickettsii.jpg" class="internal" title="Enlarge"></a></div><a href="/enwiki/wiki/Rickettsia" title="Rickettsia">Rickettsia</a> are small bacteria—here stained red—that grow in the cytoplasm of non-professional phagocytes.</div></div></div>
<p>Bacteria have developed ways to survive inside phagocytes, where they continue to evade the immune system.<sup id="cite_ref-pmid11708894_99-0" class="reference"><a href="#cite_note-pmid11708894-99">[99]</a></sup> To get safely inside the phagocyte they express proteins called <a href="/enwiki/wiki/Invasin" title="Invasin">invasins</a>. When inside the cell they remain in the cytoplasm and avoid toxic chemicals contained in the phagolysosomes.<sup id="cite_ref-pmid10064587_100-0" class="reference"><a href="#cite_note-pmid10064587-100">[100]</a></sup> Some bacteria prevent the fusion of a phagosome and lysosome, to form the phagolysosome.<sup id="cite_ref-chicken_90-3" class="reference"><a href="#cite_note-chicken-90">[90]</a></sup> Other pathogens, such as <i><a href="/enwiki/wiki/Leishmania" title="Leishmania">Leishmania</a></i>, create a highly modified <a href="/enwiki/wiki/Vacuole" title="Vacuole">vacuole</a> inside the phagocyte, which helps them persist and replicate.<sup id="cite_ref-101" class="reference"><a href="#cite_note-101">[101]</a></sup> Some bacteria are capable of living inside of the phagolysosome. <i>Staphylococcus aureus</i>, for example, produces the enzymes <a href="/enwiki/wiki/Catalase" title="Catalase">catalase</a> and <a href="/enwiki/wiki/Superoxide_dismutase" title="Superoxide dismutase">superoxide dismutase</a>, which break down chemicals—such as hydrogen peroxide—produced by phagocytes to kill bacteria.<sup id="cite_ref-pmid18607538_102-0" class="reference"><a href="#cite_note-pmid18607538-102">[102]</a></sup> Bacteria may escape from the phagosome before the formation of the phagolysosome: <i><a href="/enwiki/wiki/Listeria_monocytogenes" title="Listeria monocytogenes">Listeria monocytogenes</a></i> can make a hole in the phagosome wall using enzymes called <a href="/enwiki/wiki/Listeriolysin_O" title="Listeriolysin O">listeriolysin O</a> and <a href="/enwiki/wiki/Phospholipase_C" title="Phospholipase C">phospholipase C</a>.<sup id="cite_ref-pmid17517863_103-0" class="reference"><a href="#cite_note-pmid17517863-103">[103]</a></sup>
</p>
<h3><span class="mw-headline" id="Killing">Killing</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=23" title="Edit section: Killing">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<p>Bacteria have developed several ways of killing phagocytes.<sup id="cite_ref-pmid16322743_97-1" class="reference"><a href="#cite_note-pmid16322743-97">[97]</a></sup> These include <a href="/enwiki/wiki/Cytolysin" title="Cytolysin">cytolysins</a>, which form pores in the phagocyte's cell membranes, <a href="/enwiki/wiki/Streptolysins" class="mw-redirect" title="Streptolysins">streptolysins</a> and <a href="/enwiki/wiki/Leukocidin" title="Leukocidin">leukocidins</a>, which cause neutrophils' granules to rupture and release toxic substances,<sup id="cite_ref-pmid15819624_104-0" class="reference"><a href="#cite_note-pmid15819624-104">[104]</a></sup><sup id="cite_ref-pmid16679003_105-0" class="reference"><a href="#cite_note-pmid16679003-105">[105]</a></sup> and <a href="/enwiki/wiki/Exotoxins" class="mw-redirect" title="Exotoxins">exotoxins</a> that reduce the supply of a phagocyte's <a href="/enwiki/wiki/Adenosine_triphosphate" title="Adenosine triphosphate">ATP</a>, needed for phagocytosis. After a bacterium is ingested, it may kill the phagocyte by releasing toxins that travel through the phagosome or phagolysosome membrane to target other parts of the cell.<sup id="cite_ref-chicken_90-4" class="reference"><a href="#cite_note-chicken-90">[90]</a></sup>
</p>
<h3><span class="mw-headline" id="Disruption_of_cell_signaling">Disruption of cell signaling</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=24" title="Edit section: Disruption of cell signaling">edit</a><span class="mw-editsection-bracket">]</span></span></h3>
<div class="thumb tright"><div class="thumbinner" style="width:203px;"><a href="/enwiki/wiki/File:Leish_amast_WBC1_DPDx.JPG" class="image"><img alt="Many small cells of leishmania inside a much larger cell" src="/upwiki/wikipedia/commons/b/be/Leish_amast_WBC1_DPDx.JPG" decoding="async" width="201" height="215" class="thumbimage" data-file-width="201" data-file-height="215" /></a> <div class="thumbcaption"><div class="magnify"><a href="/enwiki/wiki/File:Leish_amast_WBC1_DPDx.JPG" class="internal" title="Enlarge"></a></div><i>Leishmania tropica</i> amastigotes (arrows) in a macrophage from skin</div></div></div>
<p>Some survival strategies often involve disrupting cytokines and other methods of <a href="/enwiki/wiki/Cell_signaling" title="Cell signaling">cell signaling</a> to prevent the phagocyte's responding to invasion.<sup id="cite_ref-pmid15639739_106-0" class="reference"><a href="#cite_note-pmid15639739-106">[106]</a></sup> The protozoan parasites <i><a href="/enwiki/wiki/Toxoplasma_gondii" title="Toxoplasma gondii">Toxoplasma gondii</a></i>, <i><a href="/enwiki/wiki/Trypanosoma_cruzi" title="Trypanosoma cruzi">Trypanosoma cruzi</a></i>, and <i><a href="/enwiki/wiki/Leishmania" title="Leishmania">Leishmania</a></i> infect macrophages, and each has a unique way of taming them.<sup id="cite_ref-pmid15639739_106-1" class="reference"><a href="#cite_note-pmid15639739-106">[106]</a></sup> Some species of <i>Leishmania</i> alter the infected macrophage's signalling, repress the production of cytokines and microbicidal molecules—nitric oxide and reactive oxygen species—and compromise antigen presentation.<sup id="cite_ref-pmid16281989_107-0" class="reference"><a href="#cite_note-pmid16281989-107">[107]</a></sup>
</p>
<h2><span class="mw-headline" id="Host_damage_by_phagocytes">Host damage by phagocytes</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=25" title="Edit section: Host damage by phagocytes">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<p>Macrophages and neutrophils, in particular, play a central role in the inflammatory process by releasing proteins and small-molecule inflammatory mediators that control infection but can damage host tissue. In general, phagocytes aim to destroy pathogens by engulfing them and subjecting them to a battery of toxic chemicals inside a <a href="/enwiki/wiki/Phagolysosome" title="Phagolysosome">phagolysosome</a>. If a phagocyte fails to engulf its target, these toxic agents can be released into the environment (an action referred to as "frustrated phagocytosis"). As these agents are also toxic to host cells, they can cause extensive damage to healthy cells and tissues.<sup id="cite_ref-108" class="reference"><a href="#cite_note-108">[108]</a></sup>
</p><p>When neutrophils release their granule contents in the <a href="/enwiki/wiki/Kidney" title="Kidney">kidney</a>, the contents of the granule (reactive oxygen compounds and proteases) degrade the <a href="/enwiki/wiki/Extracellular_matrix" title="Extracellular matrix">extracellular matrix</a> of host cells and can cause damage to <a href="/enwiki/wiki/Glomerular" class="mw-redirect" title="Glomerular">glomerular</a> cells, affecting their ability to filter blood and causing changes in shape. In addition, <a href="/enwiki/wiki/Phospholipase" title="Phospholipase">phospholipase</a> products (e.g., <a href="/enwiki/wiki/Leukotrienes" class="mw-redirect" title="Leukotrienes">leukotrienes</a>) intensify the damage. This release of substances promotes chemotaxis of more neutrophils to the site of infection, and glomerular cells can be damaged further by the adhesion molecules during the migration of neutrophils. The injury done to the glomerular cells can cause <a href="/enwiki/wiki/Kidney_failure" title="Kidney failure">kidney failure</a>.<sup id="cite_ref-pmid10430993_109-0" class="reference"><a href="#cite_note-pmid10430993-109">[109]</a></sup>
</p><p>Neutrophils also play a key role in the development of most forms of <a href="/enwiki/wiki/Acute_lung_injury" class="mw-redirect" title="Acute lung injury">acute lung injury</a>.<sup id="cite_ref-pmid11373504_110-0" class="reference"><a href="#cite_note-pmid11373504-110">[110]</a></sup> Here, activated neutrophils release the contents of their toxic granules into the lung environment.<sup id="cite_ref-pmid16319683_111-0" class="reference"><a href="#cite_note-pmid16319683-111">[111]</a></sup> Experiments have shown that a reduction in the number of neutrophils lessens the effects of acute lung injury,<sup id="cite_ref-pmid12682440_112-0" class="reference"><a href="#cite_note-pmid12682440-112">[112]</a></sup> but treatment by inhibiting neutrophils is not clinically realistic, as it would leave the host vulnerable to infection.<sup id="cite_ref-pmid16319683_111-1" class="reference"><a href="#cite_note-pmid16319683-111">[111]</a></sup> In the <a href="/enwiki/wiki/Liver" title="Liver">liver</a>, damage by neutrophils can contribute to dysfunction and injury in response to the release of <a href="/enwiki/wiki/Endotoxin" class="mw-redirect" title="Endotoxin">endotoxins</a> produced by bacteria, <a href="/enwiki/wiki/Sepsis" title="Sepsis">sepsis</a>, trauma, <a href="/enwiki/wiki/Alcoholic_hepatitis" title="Alcoholic hepatitis">alcoholic hepatitis</a>, <a href="/enwiki/wiki/Ischemia" title="Ischemia">ischemia</a>, and <a href="/enwiki/wiki/Hypovolemic_shock" title="Hypovolemic shock">hypovolemic shock</a> resulting from acute <a href="/enwiki/wiki/Hemorrhage" class="mw-redirect" title="Hemorrhage">hemorrhage</a>.<sup id="cite_ref-pmid9704069_113-0" class="reference"><a href="#cite_note-pmid9704069-113">[113]</a></sup>
</p><p>Chemicals released by macrophages can also damage host tissue. <a href="/enwiki/wiki/Tumor_necrosis_factor-alpha" class="mw-redirect" title="Tumor necrosis factor-alpha">TNF-α</a> is an important chemical that is released by macrophages that causes the blood in small vessels to clot to prevent an infection from spreading.<sup id="cite_ref-pmid17135502_114-0" class="reference"><a href="#cite_note-pmid17135502-114">[114]</a></sup> If a bacterial infection spreads to the blood, TNF-α is released into vital organs, which can cause <a href="/enwiki/wiki/Vasodilation" title="Vasodilation">vasodilation</a> and a decrease in <a href="/enwiki/wiki/Blood_plasma" title="Blood plasma">plasma</a> volume; these in turn can be followed by <a href="/enwiki/wiki/Septic_shock" title="Septic shock">septic shock</a>. During septic shock, TNF-α release causes a blockage of the small vessels that supply blood to the vital organs, and the organs may fail. Septic shock can lead to death.<sup id="cite_ref-money_50-1" class="reference"><a href="#cite_note-money-50">[50]</a></sup>
</p>
<h2><span class="mw-headline" id="Evolutionary_origins">Evolutionary origins</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=26" title="Edit section: Evolutionary origins">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<p>Phagocytosis is common and probably appeared early in <a href="/enwiki/wiki/Evolution" title="Evolution">evolution</a>,<sup id="cite_ref-115" class="reference"><a href="#cite_note-115">[115]</a></sup> evolving first in unicellular eukaryotes.<sup id="cite_ref-pmid18550419_116-0" class="reference"><a href="#cite_note-pmid18550419-116">[116]</a></sup> <a href="/enwiki/wiki/Amoeba" title="Amoeba">Amoebae</a> are unicellular <a href="/enwiki/wiki/Protists" class="mw-redirect" title="Protists">protists</a> that separated from the tree leading to <a href="/enwiki/wiki/Metazoa" class="mw-redirect" title="Metazoa">metazoa</a> shortly after the divergence of plants, and they share many specific functions with mammalian phagocytic cells.<sup id="cite_ref-pmid18550419_116-1" class="reference"><a href="#cite_note-pmid18550419-116">[116]</a></sup> <i><a href="/enwiki/wiki/Dictyostelium_discoideum" title="Dictyostelium discoideum">Dictyostelium discoideum</a></i>, for example, is an amoeba that lives in the soil and feeds on bacteria. Like animal phagocytes, it engulfs bacteria by phagocytosis mainly through Toll-like receptors, and it has other biological functions in common with macrophages.<sup id="cite_ref-pmid19081545_117-0" class="reference"><a href="#cite_note-pmid19081545-117">[117]</a></sup> <i>Dictyostelium discoideum</i> is social; it aggregates when starved to form a migrating <a href="/enwiki/wiki/Dictyostelid" title="Dictyostelid">pseudoplasmodium or slug</a>. This multicellular organism eventually will produce a <a href="/enwiki/wiki/Fruiting_body" class="mw-redirect" title="Fruiting body">fruiting body</a> with <a href="/enwiki/wiki/Spores" class="mw-redirect" title="Spores">spores</a> that are resistant to environmental dangers. Before the formation of fruiting bodies, the cells will migrate as a slug-like organism for several days. During this time, exposure to toxins or bacterial pathogens has the potential to compromise survival of the species by limiting spore production. Some of the amoebae engulf bacteria and absorb toxins while circulating within the slug, and these amoebae eventually die. They are genetically identical to the other amoebae in the slug; their self-sacrifice to protect the other amoebae from bacteria is similar to the self-sacrifice of phagocytes seen in the immune system of higher vertebrates. This ancient immune function in social amoebae suggests an evolutionarily conserved cellular foraging mechanism that might have been adapted to defense functions well before the diversification of amoebae into higher forms.<sup id="cite_ref-pmid17673666_118-0" class="reference"><a href="#cite_note-pmid17673666-118">[118]</a></sup> Phagocytes occur throughout the animal kingdom,<sup id="cite_ref-Delves250_119-0" class="reference"><a href="#cite_note-Delves250-119">[119]</a></sup> from marine sponges to insects and lower and higher vertebrates.<sup id="cite_ref-120" class="reference"><a href="#cite_note-120">[120]</a></sup><sup id="cite_ref-pmid19063916_121-0" class="reference"><a href="#cite_note-pmid19063916-121">[121]</a></sup> The ability of amoebae to distinguish between self and non-self is a pivotal one, and is the root of the immune system of many species of amoeba.<sup id="cite_ref-amoebaphage_122-0" class="reference"><a href="#cite_note-amoebaphage-122">[122]</a></sup>
</p>
<h2><span class="mw-headline" id="References">References</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=27" title="Edit section: References">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<style data-mw-deduplicate="TemplateStyles:r1011085734">.mw-parser-output .reflist{font-size:90%;margin-bottom:0.5em;list-style-type:decimal}.mw-parser-output .reflist .references{font-size:100%;margin-bottom:0;list-style-type:inherit}.mw-parser-output .reflist-columns-2{column-width:30em}.mw-parser-output .reflist-columns-3{column-width:25em}.mw-parser-output .reflist-columns{margin-top:0.3em}.mw-parser-output .reflist-columns ol{margin-top:0}.mw-parser-output .reflist-columns li{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .reflist-upper-alpha{list-style-type:upper-alpha}.mw-parser-output .reflist-upper-roman{list-style-type:upper-roman}.mw-parser-output .reflist-lower-alpha{list-style-type:lower-alpha}.mw-parser-output .reflist-lower-greek{list-style-type:lower-greek}.mw-parser-output .reflist-lower-roman{list-style-type:lower-roman}</style><div class="reflist reflist-columns references-column-width" style="column-width: 30em;">
<ol class="references">
<li id="cite_note-1"><span class="mw-cite-backlink"><b><a href="#cite_ref-1">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 6–7</span>
</li>
<li id="cite_note-pmid8301210-2"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid8301210_2-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>pmid8301210</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-3"><span class="mw-cite-backlink"><b><a href="#cite_ref-3">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 2</span>
</li>
<li id="cite_note-4"><span class="mw-cite-backlink"><b><a href="#cite_ref-4">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 2</span>
</li>
<li id="cite_note-USC-5"><span class="mw-cite-backlink">^ <a href="#cite_ref-USC_5-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-USC_5-1"><sup><i><b>b</b></i></sup></a> <a href="#cite_ref-USC_5-2"><sup><i><b>c</b></i></sup></a> <a href="#cite_ref-USC_5-3"><sup><i><b>d</b></i></sup></a> <a href="#cite_ref-USC_5-4"><sup><i><b>e</b></i></sup></a> <a href="#cite_ref-USC_5-5"><sup><i><b>f</b></i></sup></a> <a href="#cite_ref-USC_5-6"><sup><i><b>g</b></i></sup></a> <a href="#cite_ref-USC_5-7"><sup><i><b>h</b></i></sup></a></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>USC</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-6"><span class="mw-cite-backlink"><b><a href="#cite_ref-6">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, pp. 13–16</span>
</li>
<li id="cite_note-pmid18684880-7"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18684880_7-0">^</a></b></span> <span class="reference-text"><style data-mw-deduplicate="TemplateStyles:r1067248974">.mw-parser-output cite.citation{font-style:inherit;word-wrap:break-word}.mw-parser-output .citation q{quotes:"\"""\"""'""'"}.mw-parser-output .citation:target{background-color:rgba(0,127,255,0.133)}.mw-parser-output .id-lock-free a,.mw-parser-output .citation .cs1-lock-free a{background:linear-gradient(transparent,transparent),url("/upwiki/wikipedia/commons/6/65/Lock-green.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-limited a,.mw-parser-output .id-lock-registration a,.mw-parser-output .citation .cs1-lock-limited a,.mw-parser-output .citation .cs1-lock-registration a{background:linear-gradient(transparent,transparent),url("/upwiki/wikipedia/commons/d/d6/Lock-gray-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-subscription a,.mw-parser-output .citation .cs1-lock-subscription a{background:linear-gradient(transparent,transparent),url("/upwiki/wikipedia/commons/a/aa/Lock-red-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .cs1-ws-icon a{background:linear-gradient(transparent,transparent),url("/upwiki/wikipedia/commons/4/4c/Wikisource-logo.svg")right 0.1em center/12px no-repeat}.mw-parser-output .cs1-code{color:inherit;background:inherit;border:none;padding:inherit}.mw-parser-output .cs1-hidden-error{display:none;color:#d33}.mw-parser-output .cs1-visible-error{color:#d33}.mw-parser-output .cs1-maint{display:none;color:#3a3;margin-left:0.3em}.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right{padding-right:0.2em}.mw-parser-output .citation .mw-selflink{font-weight:inherit}</style><cite id="CITEREFDale_DC,_Boxer_L,_Liles_WCBoxerLiles2008" class="citation journal cs1">Dale DC, Boxer L, Liles WC; Boxer; Liles (August 2008). <a rel="nofollow" class="external text" href="https://doi.org/10.1182%2Fblood-2007-12-077917">"The phagocytes: neutrophils and monocytes"</a>. <i>Blood</i>. <b>112</b> (4): 935–45. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1182%2Fblood-2007-12-077917">10.1182/blood-2007-12-077917</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18684880">18684880</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:746699">746699</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Blood&rft.atitle=The+phagocytes%3A+neutrophils+and+monocytes&rft.volume=112&rft.issue=4&rft.pages=935-45&rft.date=2008-08&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A746699%23id-name%3DS2CID&rft_id=info%3Apmid%2F18684880&rft_id=info%3Adoi%2F10.1182%2Fblood-2007-12-077917&rft.au=Dale+DC%2C+Boxer+L%2C+Liles+WC&rft.au=Boxer&rft.au=Liles&rft_id=%2F%2Fdoi.org%2F10.1182%252Fblood-2007-12-077917&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-8"><span class="mw-cite-backlink"><b><a href="#cite_ref-8">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFDahlgrenA_Karlsson1999" class="citation journal cs1">Dahlgren, C; A Karlsson (December 17, 1999). "Respiratory burst in human neutrophils". <i>Journal of Immunological Methods</i>. <b>232</b> (1–2): 3–14. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS0022-1759%2899%2900146-5">10.1016/S0022-1759(99)00146-5</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/10618505">10618505</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Journal+of+Immunological+Methods&rft.atitle=Respiratory+burst+in+human+neutrophils&rft.volume=232&rft.issue=1%E2%80%932&rft.pages=3-14&rft.date=1999-12-17&rft_id=info%3Adoi%2F10.1016%2FS0022-1759%2899%2900146-5&rft_id=info%3Apmid%2F10618505&rft.aulast=Dahlgren&rft.aufirst=C&rft.au=A+Karlsson&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid15378046-9"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid15378046_9-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>pmid15378046</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-10"><span class="mw-cite-backlink"><b><a href="#cite_ref-10">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFShatwellAW_Segal1996" class="citation journal cs1">Shatwell, KP; AW Segal (1996). "NADPH oxidase". <i>The International Journal of Biochemistry & Cell Biology</i>. <b>28</b> (11): 1191–95. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS1357-2725%2896%2900084-2">10.1016/S1357-2725(96)00084-2</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/9022278">9022278</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=The+International+Journal+of+Biochemistry+%26+Cell+Biology&rft.atitle=NADPH+oxidase&rft.volume=28&rft.issue=11&rft.pages=1191-95&rft.date=1996&rft_id=info%3Adoi%2F10.1016%2FS1357-2725%2896%2900084-2&rft_id=info%3Apmid%2F9022278&rft.aulast=Shatwell&rft.aufirst=KP&rft.au=AW+Segal&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid10519157-11"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid10519157_11-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFKlebanoff_SJ1999" class="citation journal cs1">Klebanoff SJ (1999). "Myeloperoxidase". <i>Proc. Assoc. Am. Physicians</i>. <b>111</b> (5): 383–89. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1111%2Fpaa.1999.111.5.383">10.1111/paa.1999.111.5.383</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/10519157">10519157</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Proc.+Assoc.+Am.+Physicians&rft.atitle=Myeloperoxidase&rft.volume=111&rft.issue=5&rft.pages=383-89&rft.date=1999&rft_id=info%3Adoi%2F10.1111%2Fpaa.1999.111.5.383&rft_id=info%3Apmid%2F10519157&rft.au=Klebanoff+SJ&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid15478278-12"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid15478278_12-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFMeyer_KC2004" class="citation journal cs1">Meyer KC (September 2004). "Neutrophils, myeloperoxidase, and bronchiectasis in cystic fibrosis: green is not good". <i>J. Lab. Clin. Med</i>. <b>144</b> (3): 124–26. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.lab.2004.05.014">10.1016/j.lab.2004.05.014</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/15478278">15478278</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Lab.+Clin.+Med.&rft.atitle=Neutrophils%2C+myeloperoxidase%2C+and+bronchiectasis+in+cystic+fibrosis%3A+green+is+not+good&rft.volume=144&rft.issue=3&rft.pages=124-26&rft.date=2004-09&rft_id=info%3Adoi%2F10.1016%2Fj.lab.2004.05.014&rft_id=info%3Apmid%2F15478278&rft.au=Meyer+KC&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-13"><span class="mw-cite-backlink"><b><a href="#cite_ref-13">^</a></b></span> <span class="reference-text"><a href="#CITEREFHoffbrandPettitMoss2005">Hoffbrand, Pettit & Moss 2005</a>, p. 118</span>
</li>
<li id="cite_note-14"><span class="mw-cite-backlink"><b><a href="#cite_ref-14">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 6–10</span>
</li>
<li id="cite_note-pmid14525967-15"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid14525967_15-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSchroder_K,_Hertzog_PJ,_Ravasi_T,_Hume_DAHertzogRavasiHume2004" class="citation journal cs1">Schroder K, Hertzog PJ, Ravasi T, Hume DA; Hertzog; Ravasi; Hume (February 2004). <a rel="nofollow" class="external text" href="https://doi.org/10.1189%2Fjlb.0603252">"Interferon-gamma: an overview of signals, mechanisms and functions"</a>. <i>J. Leukoc. Biol</i>. <b>75</b> (2): 163–89. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1189%2Fjlb.0603252">10.1189/jlb.0603252</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/14525967">14525967</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:15862242">15862242</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Leukoc.+Biol.&rft.atitle=Interferon-gamma%3A+an+overview+of+signals%2C+mechanisms+and+functions&rft.volume=75&rft.issue=2&rft.pages=163-89&rft.date=2004-02&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A15862242%23id-name%3DS2CID&rft_id=info%3Apmid%2F14525967&rft_id=info%3Adoi%2F10.1189%2Fjlb.0603252&rft.au=Schroder+K%2C+Hertzog+PJ%2C+Ravasi+T%2C+Hume+DA&rft.au=Hertzog&rft.au=Ravasi&rft.au=Hume&rft_id=%2F%2Fdoi.org%2F10.1189%252Fjlb.0603252&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-16"><span class="mw-cite-backlink"><b><a href="#cite_ref-16">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, p. 188</span>
</li>
<li id="cite_note-autogenerated2-17"><span class="mw-cite-backlink">^ <a href="#cite_ref-autogenerated2_17-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-autogenerated2_17-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 136</span>
</li>
<li id="cite_note-pmid18846805-18"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18846805_18-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFLipu_HN,_Ahmed_TA,_Ali_S,_Ahmed_D,_Waqar_MAAhmedAliAhmed2008" class="citation journal cs1">Lipu HN, Ahmed TA, Ali S, Ahmed D, Waqar MA; Ahmed; Ali; Ahmed; Waqar (September 2008). "Chronic granulomatous disease". <i>J Pak Med Assoc</i>. <b>58</b> (9): 516–18. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18846805">18846805</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J+Pak+Med+Assoc&rft.atitle=Chronic+granulomatous+disease&rft.volume=58&rft.issue=9&rft.pages=516-18&rft.date=2008-09&rft_id=info%3Apmid%2F18846805&rft.au=Lipu+HN%2C+Ahmed+TA%2C+Ali+S%2C+Ahmed+D%2C+Waqar+MA&rft.au=Ahmed&rft.au=Ali&rft.au=Ahmed&rft.au=Waqar&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid18043242-19"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18043242_19-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFKaplan_J,_De_Domenico_I,_Ward_DMDe_DomenicoWard2008" class="citation journal cs1">Kaplan J, De Domenico I, Ward DM; De Domenico; Ward (January 2008). "Chediak-Higashi syndrome". <i>Curr. Opin. Hematol</i>. <b>15</b> (1): 22–29. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1097%2FMOH.0b013e3282f2bcce">10.1097/MOH.0b013e3282f2bcce</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18043242">18043242</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:43243529">43243529</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Curr.+Opin.+Hematol.&rft.atitle=Chediak-Higashi+syndrome&rft.volume=15&rft.issue=1&rft.pages=22-29&rft.date=2008-01&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A43243529%23id-name%3DS2CID&rft_id=info%3Apmid%2F18043242&rft_id=info%3Adoi%2F10.1097%2FMOH.0b013e3282f2bcce&rft.au=Kaplan+J%2C+De+Domenico+I%2C+Ward+DM&rft.au=De+Domenico&rft.au=Ward&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-20"><span class="mw-cite-backlink"><b><a href="#cite_ref-20">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 7</span>
</li>
<li id="cite_note-pmid17962876-21"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid17962876_21-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFde_Almeida_SM,_Nogueira_MB,_Raboni_SM,_Vidal_LRNogueiraRaboniVidal2007" class="citation journal cs1">de Almeida SM, Nogueira MB, Raboni SM, Vidal LR; Nogueira; Raboni; Vidal (October 2007). <a rel="nofollow" class="external text" href="https://doi.org/10.1590%2Fs1413-86702007000500010">"Laboratorial diagnosis of lymphocytic meningitis"</a>. <i>Braz J Infect Dis</i>. <b>11</b> (5): 489–95. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1590%2Fs1413-86702007000500010">10.1590/s1413-86702007000500010</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17962876">17962876</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Braz+J+Infect+Dis&rft.atitle=Laboratorial+diagnosis+of+lymphocytic+meningitis&rft.volume=11&rft.issue=5&rft.pages=489-95&rft.date=2007-10&rft_id=info%3Adoi%2F10.1590%2Fs1413-86702007000500010&rft_id=info%3Apmid%2F17962876&rft.au=de+Almeida+SM%2C+Nogueira+MB%2C+Raboni+SM%2C+Vidal+LR&rft.au=Nogueira&rft.au=Raboni&rft.au=Vidal&rft_id=%2F%2Fdoi.org%2F10.1590%252Fs1413-86702007000500010&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-22"><span class="mw-cite-backlink"><b><a href="#cite_ref-22">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 22</span>
</li>
<li id="cite_note-pathogenesis-23"><span class="mw-cite-backlink"><b><a href="#cite_ref-pathogenesis_23-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFThompson,_CB1995" class="citation journal cs1">Thompson, CB (1995). "Apoptosis in the pathogenesis and treatment of disease". <i>Science</i>. <b>267</b> (5203): 1456–62. <a href="/enwiki/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/1995Sci...267.1456T">1995Sci...267.1456T</a>. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1126%2Fscience.7878464">10.1126/science.7878464</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/7878464">7878464</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:12991980">12991980</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Apoptosis+in+the+pathogenesis+and+treatment+of+disease&rft.volume=267&rft.issue=5203&rft.pages=1456-62&rft.date=1995&rft_id=info%3Adoi%2F10.1126%2Fscience.7878464&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A12991980%23id-name%3DS2CID&rft_id=info%3Apmid%2F7878464&rft_id=info%3Abibcode%2F1995Sci...267.1456T&rft.au=Thompson%2C+CB&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-24"><span class="mw-cite-backlink"><b><a href="#cite_ref-24">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 68</span>
</li>
<li id="cite_note-25"><span class="mw-cite-backlink"><b><a href="#cite_ref-25">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite class="citation web cs1"><a rel="nofollow" class="external text" href="http://www.merriam-webster.com/dictionary/apoptosis">"Apoptosis"</a>. <i>Merriam-Webster Online Dictionary</i><span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=unknown&rft.jtitle=Merriam-Webster+Online+Dictionary&rft.atitle=Apoptosis&rft_id=http%3A%2F%2Fwww.merriam-webster.com%2Fdictionary%2Fapoptosis&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid14645847-26"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid14645847_26-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFLi_MO,_Sarkisian_MR,_Mehal_WZ,_Rakic_P,_Flavell_RASarkisianMehalRakic2003" class="citation journal cs1">Li MO, Sarkisian MR, Mehal WZ, Rakic P, Flavell RA; Sarkisian; Mehal; Rakic; Flavell (November 2003). <a rel="nofollow" class="external text" href="https://semanticscholar.org/paper/0946eda3ac2cb65b78a7af7b879f97db91c7023a">"Phosphatidylserine receptor is required for clearance of apoptotic cells"</a>. <i>Science</i>. <b>302</b> (5650): 1560–63. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1126%2Fscience.1087621">10.1126/science.1087621</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/14645847">14645847</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:36252352">36252352</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Phosphatidylserine+receptor+is+required+for+clearance+of+apoptotic+cells&rft.volume=302&rft.issue=5650&rft.pages=1560-63&rft.date=2003-11&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A36252352%23id-name%3DS2CID&rft_id=info%3Apmid%2F14645847&rft_id=info%3Adoi%2F10.1126%2Fscience.1087621&rft.au=Li+MO%2C+Sarkisian+MR%2C+Mehal+WZ%2C+Rakic+P%2C+Flavell+RA&rft.au=Sarkisian&rft.au=Mehal&rft.au=Rakic&rft.au=Flavell&rft_id=https%3A%2F%2Fsemanticscholar.org%2Fpaper%2F0946eda3ac2cb65b78a7af7b879f97db91c7023a&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span> (Free registration required for online access)</span>
</li>
<li id="cite_note-pmid31837595-27"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid31837595_27-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFNagataSakuragiSegawa2019" class="citation journal cs1">Nagata S, Sakuragi T, Segawa K (December 2019). <a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.coi.2019.11.009">"Flippase and scramblase for phosphatidylserine exposure"</a>. <i>Current Opinion in Immunology</i>. <b>62</b>: 31–38. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.coi.2019.11.009">10.1016/j.coi.2019.11.009</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/31837595">31837595</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Current+Opinion+in+Immunology&rft.atitle=Flippase+and+scramblase+for+phosphatidylserine+exposure&rft.volume=62&rft.pages=31-38&rft.date=2019-12&rft_id=info%3Adoi%2F10.1016%2Fj.coi.2019.11.009&rft_id=info%3Apmid%2F31837595&rft.aulast=Nagata&rft.aufirst=S&rft.au=Sakuragi%2C+T&rft.au=Segawa%2C+K&rft_id=%2F%2Fdoi.org%2F10.1016%252Fj.coi.2019.11.009&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-phago2-28"><span class="mw-cite-backlink"><b><a href="#cite_ref-phago2_28-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFWang_X2003" class="citation journal cs1">Wang X (2003). <a rel="nofollow" class="external text" href="https://semanticscholar.org/paper/ca6fd5581faa5fa9ee33ab1a2d993a910188788c">"Cell corpse engulfment mediated by <i>C. elegans</i> phosphatidylserine receptor through CED-5 and CED-12"</a>. <i>Science</i>. <b>302</b> (5650): 1563–1566. <a href="/enwiki/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/2003Sci...302.1563W">2003Sci...302.1563W</a>. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1126%2Fscience.1087641">10.1126/science.1087641</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/14645848">14645848</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:25672278">25672278</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Cell+corpse+engulfment+mediated+by+C.+elegans+phosphatidylserine+receptor+through+CED-5+and+CED-12&rft.volume=302&rft.issue=5650&rft.pages=1563-1566&rft.date=2003&rft_id=info%3Adoi%2F10.1126%2Fscience.1087641&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A25672278%23id-name%3DS2CID&rft_id=info%3Apmid%2F14645848&rft_id=info%3Abibcode%2F2003Sci...302.1563W&rft.au=Wang+X&rft_id=https%3A%2F%2Fsemanticscholar.org%2Fpaper%2Fca6fd5581faa5fa9ee33ab1a2d993a910188788c&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span> (Free registration required for online access)</span>
</li>
<li id="cite_note-phago1-29"><span class="mw-cite-backlink"><b><a href="#cite_ref-phago1_29-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSavillGregoryHaslett2003" class="citation journal cs1">Savill J, Gregory C, Haslett C (2003). <a rel="nofollow" class="external text" href="https://semanticscholar.org/paper/da2238a1c09adaca71a04c8c04305a189db6c865">"Eat me or die"</a>. <i>Science</i>. <b>302</b> (5650): 1516–17. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1126%2Fscience.1092533">10.1126/science.1092533</a>. <a href="/enwiki/wiki/Hdl_(identifier)" class="mw-redirect" title="Hdl (identifier)">hdl</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//hdl.handle.net/1842%2F448">1842/448</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/14645835">14645835</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:13402617">13402617</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Eat+me+or+die&rft.volume=302&rft.issue=5650&rft.pages=1516-17&rft.date=2003&rft_id=info%3Ahdl%2F1842%2F448&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A13402617%23id-name%3DS2CID&rft_id=info%3Apmid%2F14645835&rft_id=info%3Adoi%2F10.1126%2Fscience.1092533&rft.aulast=Savill&rft.aufirst=J&rft.au=Gregory%2C+C&rft.au=Haslett%2C+C&rft_id=https%3A%2F%2Fsemanticscholar.org%2Fpaper%2Fda2238a1c09adaca71a04c8c04305a189db6c865&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid18774293-30"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18774293_30-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFZhou_Z,_Yu_XYu2008" class="citation journal cs1">Zhou Z, Yu X; Yu (October 2008). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3125982">"Phagosome maturation during the removal of apoptotic cells: receptors lead the way"</a>. <i>Trends Cell Biol</i>. <b>18</b> (10): 474–85. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.tcb.2008.08.002">10.1016/j.tcb.2008.08.002</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3125982">3125982</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18774293">18774293</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Trends+Cell+Biol.&rft.atitle=Phagosome+maturation+during+the+removal+of+apoptotic+cells%3A+receptors+lead+the+way&rft.volume=18&rft.issue=10&rft.pages=474-85&rft.date=2008-10&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3125982%23id-name%3DPMC&rft_id=info%3Apmid%2F18774293&rft_id=info%3Adoi%2F10.1016%2Fj.tcb.2008.08.002&rft.au=Zhou+Z%2C+Yu+X&rft.au=Yu&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3125982&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-31"><span class="mw-cite-backlink"><b><a href="#cite_ref-31">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 3</span>
</li>
<li id="cite_note-32"><span class="mw-cite-backlink"><b><a href="#cite_ref-32">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 4</span>
</li>
<li id="cite_note-33"><span class="mw-cite-backlink"><b><a href="#cite_ref-33">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, pp. 27–35</span>
</li>
<li id="cite_note-34"><span class="mw-cite-backlink"><b><a href="#cite_ref-34">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 171–184</span>
</li>
<li id="cite_note-35"><span class="mw-cite-backlink"><b><a href="#cite_ref-35">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 456</span>
</li>
<li id="cite_note-paper-36"><span class="mw-cite-backlink"><b><a href="#cite_ref-paper_36-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFTimothy_Lee2004" class="citation web cs1">Timothy Lee (2004). <a rel="nofollow" class="external text" href="https://web.archive.org/web/20080112211805/http://pim.medicine.dal.ca/apc.htm">"Antigen Presenting Cells (APC)"</a>. <i>Immunology for 1st Year Medical Students</i>. Dalhousie University. Archived from <a rel="nofollow" class="external text" href="http://pim.medicine.dal.ca/apc.htm">the original</a> on January 12, 2008<span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=unknown&rft.jtitle=Immunology+for+1st+Year+Medical+Students&rft.atitle=Antigen+Presenting+Cells+%28APC%29&rft.date=2004&rft.au=Timothy+Lee&rft_id=http%3A%2F%2Fpim.medicine.dal.ca%2Fapc.htm&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-ATP-37"><span class="mw-cite-backlink"><b><a href="#cite_ref-ATP_37-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>ATP</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-38"><span class="mw-cite-backlink"><b><a href="#cite_ref-38">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, p. 161</span>
</li>
<li id="cite_note-39"><span class="mw-cite-backlink"><b><a href="#cite_ref-39">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 8</span>
</li>
<li id="cite_note-40"><span class="mw-cite-backlink"><b><a href="#cite_ref-40">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 237–242</span>
</li>
<li id="cite_note-somethingcool-41"><span class="mw-cite-backlink"><b><a href="#cite_ref-somethingcool_41-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFLange_C,_Dürr_M,_Doster_H,_Melms_A,_Bischof_FDürrDosterMelms2007" class="citation journal cs1">Lange C, Dürr M, Doster H, Melms A, Bischof F; Dürr; Doster; Melms; Bischof (2007). "Dendritic cell-regulatory T-cell interactions control self-directed immunity". <i>Immunol. Cell Biol</i>. <b>85</b> (8): 575–81. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fsj.icb.7100088">10.1038/sj.icb.7100088</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17592494">17592494</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:36342899">36342899</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Immunol.+Cell+Biol.&rft.atitle=Dendritic+cell-regulatory+T-cell+interactions+control+self-directed+immunity&rft.volume=85&rft.issue=8&rft.pages=575-81&rft.date=2007&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A36342899%23id-name%3DS2CID&rft_id=info%3Apmid%2F17592494&rft_id=info%3Adoi%2F10.1038%2Fsj.icb.7100088&rft.au=Lange+C%2C+D%C3%BCrr+M%2C+Doster+H%2C+Melms+A%2C+Bischof+F&rft.au=D%C3%BCrr&rft.au=Doster&rft.au=Melms&rft.au=Bischof&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-rocky-42"><span class="mw-cite-backlink"><b><a href="#cite_ref-rocky_42-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSteinman2004" class="citation web cs1">Steinman, Ralph M. (2004). <a rel="nofollow" class="external text" href="https://web.archive.org/web/20090311032056/http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php">"Dendritic Cells and Immune Tolerance"</a>. The Rockefeller University. Archived from <a rel="nofollow" class="external text" href="http://www.rockefeller.edu/labheads/steinman/dendritic_intro/immuneTolerance.php">the original</a> on March 11, 2009<span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=unknown&rft.btitle=Dendritic+Cells+and+Immune+Tolerance&rft.pub=The+Rockefeller+University&rft.date=2004&rft.aulast=Steinman&rft.aufirst=Ralph+M.&rft_id=http%3A%2F%2Fwww.rockefeller.edu%2Flabheads%2Fsteinman%2Fdendritic_intro%2FimmuneTolerance.php&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-43"><span class="mw-cite-backlink"><b><a href="#cite_ref-43">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFRomagnani2006" class="citation journal cs1">Romagnani, S (2006). "Immunological tolerance and autoimmunity". <i>Internal and Emergency Medicine</i>. <b>1</b> (3): 187–96. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1007%2FBF02934736">10.1007/BF02934736</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17120464">17120464</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:27585046">27585046</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Internal+and+Emergency+Medicine&rft.atitle=Immunological+tolerance+and+autoimmunity&rft.volume=1&rft.issue=3&rft.pages=187-96&rft.date=2006&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A27585046%23id-name%3DS2CID&rft_id=info%3Apmid%2F17120464&rft_id=info%3Adoi%2F10.1007%2FBF02934736&rft.aulast=Romagnani&rft.aufirst=S&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-Ernst186-44"><span class="mw-cite-backlink"><b><a href="#cite_ref-Ernst186_44-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>Ernst186</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-Rob-45"><span class="mw-cite-backlink"><b><a href="#cite_ref-Rob_45-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>Rob</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-Hoff-values-46"><span class="mw-cite-backlink">^ <a href="#cite_ref-Hoff-values_46-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-Hoff-values_46-1"><sup><i><b>b</b></i></sup></a> <a href="#cite_ref-Hoff-values_46-2"><sup><i><b>c</b></i></sup></a></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>Hoff-values</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-47"><span class="mw-cite-backlink"><b><a href="#cite_ref-47">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, pp. 16–17</span>
</li>
<li id="cite_note-48"><span class="mw-cite-backlink"><b><a href="#cite_ref-48">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, pp. 18–19</span>
</li>
<li id="cite_note-49"><span class="mw-cite-backlink"><b><a href="#cite_ref-49">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, p. 6</span>
</li>
<li id="cite_note-money-50"><span class="mw-cite-backlink">^ <a href="#cite_ref-money_50-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-money_50-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text">Janeway, Chapter: <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=migration&rid=imm.section.203#206">Induced innate responses to infection.</a></span>
</li>
<li id="cite_note-pmid14519390-51"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid14519390_51-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFZen_K,_Parkos_CAParkos2003" class="citation journal cs1">Zen K, Parkos CA; Parkos (October 2003). "Leukocyte-epithelial interactions". <i>Curr. Opin. Cell Biol</i>. <b>15</b> (5): 557–64. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS0955-0674%2803%2900103-0">10.1016/S0955-0674(03)00103-0</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/14519390">14519390</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Curr.+Opin.+Cell+Biol.&rft.atitle=Leukocyte-epithelial+interactions&rft.volume=15&rft.issue=5&rft.pages=557-64&rft.date=2003-10&rft_id=info%3Adoi%2F10.1016%2FS0955-0674%2803%2900103-0&rft_id=info%3Apmid%2F14519390&rft.au=Zen+K%2C+Parkos+CA&rft.au=Parkos&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-52"><span class="mw-cite-backlink"><b><a href="#cite_ref-52">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 18</span>
</li>
<li id="cite_note-53"><span class="mw-cite-backlink"><b><a href="#cite_ref-53">^</a></b></span> <span class="reference-text"><a href="#CITEREFHoffbrandPettitMoss2005">Hoffbrand, Pettit & Moss 2005</a>, p. 117</span>
</li>
<li id="cite_note-54"><span class="mw-cite-backlink"><b><a href="#cite_ref-54">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 1–6</span>
</li>
<li id="cite_note-55"><span class="mw-cite-backlink"><b><a href="#cite_ref-55">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 136</span>
</li>
<li id="cite_note-pmid8870002-56"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid8870002_56-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFTakahashi_K,_Naito_M,_Takeya_MNaitoTakeya1996" class="citation journal cs1">Takahashi K, Naito M, Takeya M; Naito; Takeya (July 1996). "Development and heterogeneity of macrophages and their related cells through their differentiation pathways". <i>Pathol. Int</i>. <b>46</b> (7): 473–85. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1111%2Fj.1440-1827.1996.tb03641.x">10.1111/j.1440-1827.1996.tb03641.x</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/8870002">8870002</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:6049656">6049656</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Pathol.+Int.&rft.atitle=Development+and+heterogeneity+of+macrophages+and+their+related+cells+through+their+differentiation+pathways&rft.volume=46&rft.issue=7&rft.pages=473-85&rft.date=1996-07&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A6049656%23id-name%3DS2CID&rft_id=info%3Apmid%2F8870002&rft_id=info%3Adoi%2F10.1111%2Fj.1440-1827.1996.tb03641.x&rft.au=Takahashi+K%2C+Naito+M%2C+Takeya+M&rft.au=Naito&rft.au=Takeya&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-57"><span class="mw-cite-backlink"><b><a href="#cite_ref-57">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFKrombach_F,_Münzing_S,_Allmeling_AM,_Gerlach_JT,_Behr_J,_Dörger_MMünzingAllmelingGerlach1997" class="citation journal cs1 cs1-prop-long-vol">Krombach F, Münzing S, Allmeling AM, Gerlach JT, Behr J, Dörger M; Münzing; Allmeling; Gerlach; Behr; Dörger (September 1997). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC1470168">"Cell size of alveolar macrophages: an interspecies comparison"</a>. <i>Environ. Health Perspect</i>. 105 Suppl 5 (Suppl 5): 1261–63. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.2307%2F3433544">10.2307/3433544</a>. <a href="/enwiki/wiki/JSTOR_(identifier)" class="mw-redirect" title="JSTOR (identifier)">JSTOR</a> <a rel="nofollow" class="external text" href="/enwiki//www.jstor.org/stable/3433544">3433544</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC1470168">1470168</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/9400735">9400735</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Environ.+Health+Perspect.&rft.atitle=Cell+size+of+alveolar+macrophages%3A+an+interspecies+comparison&rft.volume=105+Suppl+5&rft.issue=Suppl+5&rft.pages=1261-63&rft.date=1997-09&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1470168%23id-name%3DPMC&rft_id=info%3Apmid%2F9400735&rft_id=%2F%2Fwww.jstor.org%2Fstable%2F3433544%23id-name%3DJSTOR&rft_id=info%3Adoi%2F10.2307%2F3433544&rft.au=Krombach+F%2C+M%C3%BCnzing+S%2C+Allmeling+AM%2C+Gerlach+JT%2C+Behr+J%2C+D%C3%B6rger+M&rft.au=M%C3%BCnzing&rft.au=Allmeling&rft.au=Gerlach&rft.au=Behr&rft.au=D%C3%B6rger&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1470168&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-USCmac-58"><span class="mw-cite-backlink">^ <a href="#cite_ref-USCmac_58-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-USCmac_58-1"><sup><i><b>b</b></i></sup></a> <a href="#cite_ref-USCmac_58-2"><sup><i><b>c</b></i></sup></a> <a href="#cite_ref-USCmac_58-3"><sup><i><b>d</b></i></sup></a> <a href="#cite_ref-USCmac_58-4"><sup><i><b>e</b></i></sup></a></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 31–36</span>
</li>
<li id="cite_note-59"><span class="mw-cite-backlink"><b><a href="#cite_ref-59">^</a></b></span> <span class="reference-text"><a href="#CITEREFErnstStendahl2006">Ernst & Stendahl 2006</a>, p. 8</span>
</li>
<li id="cite_note-60"><span class="mw-cite-backlink"><b><a href="#cite_ref-60">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, p. 156</span>
</li>
<li id="cite_note-61"><span class="mw-cite-backlink"><b><a href="#cite_ref-61">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, p. 187</span>
</li>
<li id="cite_note-IandF-62"><span class="mw-cite-backlink"><b><a href="#cite_ref-IandF_62-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFStvrtinováJán_Jakubovský_and_Ivan_Hulín1995" class="citation book cs1">Stvrtinová, Viera; Ján Jakubovský and Ivan Hulín (1995). <a rel="nofollow" class="external text" href="https://web.archive.org/web/20101231014453/http://nic.sav.sk/logos/books/scientific/node15.html">"Neutrophils, central cells in acute inflammation"</a>. <i>Inflammation and Fever from Pathophysiology: Principles of Disease</i>. Computing Centre, Slovak Academy of Sciences: Academic Electronic Press. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-80-967366-1-4" title="Special:BookSources/978-80-967366-1-4"><bdi>978-80-967366-1-4</bdi></a>. Archived from <a rel="nofollow" class="external text" href="http://nic.sav.sk/logos/books/scientific/node15.html">the original</a> on December 31, 2010<span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=bookitem&rft.atitle=Neutrophils%2C+central+cells+in+acute+inflammation&rft.btitle=Inflammation+and+Fever+from+Pathophysiology%3A+Principles+of+Disease&rft.place=Computing+Centre%2C+Slovak+Academy+of+Sciences&rft.pub=Academic+Electronic+Press&rft.date=1995&rft.isbn=978-80-967366-1-4&rft.aulast=Stvrtinov%C3%A1&rft.aufirst=Viera&rft.au=J%C3%A1n+Jakubovsk%C3%BD+and+Ivan+Hul%C3%ADn&rft_id=http%3A%2F%2Fnic.sav.sk%2Flogos%2Fbooks%2Fscientific%2Fnode15.html&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-63"><span class="mw-cite-backlink"><b><a href="#cite_ref-63">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, p. 4</span>
</li>
<li id="cite_note-Som18-64"><span class="mw-cite-backlink">^ <a href="#cite_ref-Som18_64-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-Som18_64-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 18</span>
</li>
<li id="cite_note-pmid9853933-65"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid9853933_65-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFLinderkamp_O,_Ruef_P,_Brenner_B,_Gulbins_E,_Lang_FRuefBrennerGulbins1998" class="citation journal cs1">Linderkamp O, Ruef P, Brenner B, Gulbins E, Lang F; Ruef; Brenner; Gulbins; Lang (December 1998). <a rel="nofollow" class="external text" href="https://doi.org/10.1203%2F00006450-199812000-00021">"Passive deformability of mature, immature, and active neutrophils in healthy and septicemic neonates"</a>. <i>Pediatr. Res</i>. <b>44</b> (6): 946–50. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1203%2F00006450-199812000-00021">10.1203/00006450-199812000-00021</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/9853933">9853933</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Pediatr.+Res.&rft.atitle=Passive+deformability+of+mature%2C+immature%2C+and+active+neutrophils+in+healthy+and+septicemic+neonates&rft.volume=44&rft.issue=6&rft.pages=946-50&rft.date=1998-12&rft_id=info%3Adoi%2F10.1203%2F00006450-199812000-00021&rft_id=info%3Apmid%2F9853933&rft.au=Linderkamp+O%2C+Ruef+P%2C+Brenner+B%2C+Gulbins+E%2C+Lang+F&rft.au=Ruef&rft.au=Brenner&rft.au=Gulbins&rft.au=Lang&rft_id=%2F%2Fdoi.org%2F10.1203%252F00006450-199812000-00021&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-66"><span class="mw-cite-backlink"><b><a href="#cite_ref-66">^</a></b></span> <span class="reference-text"><a href="#CITEREFPaolettiNotarioRicevuti1997">Paoletti, Notario & Ricevuti 1997</a>, p. 62</span>
</li>
<li id="cite_note-pmid17991288-67"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid17991288_67-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSoehnlein_O,_Kenne_E,_Rotzius_P,_Eriksson_EE,_Lindbom_LKenneRotziusEriksson2008" class="citation journal cs1">Soehnlein O, Kenne E, Rotzius P, Eriksson EE, Lindbom L; Kenne; Rotzius; Eriksson; Lindbom (January 2008). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2276935">"Neutrophil secretion products regulate anti-bacterial activity in monocytes and macrophages"</a>. <i>Clin. Exp. Immunol</i>. <b>151</b> (1): 139–45. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1111%2Fj.1365-2249.2007.03532.x">10.1111/j.1365-2249.2007.03532.x</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2276935">2276935</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17991288">17991288</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Clin.+Exp.+Immunol.&rft.atitle=Neutrophil+secretion+products+regulate+anti-bacterial+activity+in+monocytes+and+macrophages&rft.volume=151&rft.issue=1&rft.pages=139-45&rft.date=2008-01&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2276935%23id-name%3DPMC&rft_id=info%3Apmid%2F17991288&rft_id=info%3Adoi%2F10.1111%2Fj.1365-2249.2007.03532.x&rft.au=Soehnlein+O%2C+Kenne+E%2C+Rotzius+P%2C+Eriksson+EE%2C+Lindbom+L&rft.au=Kenne&rft.au=Rotzius&rft.au=Eriksson&rft.au=Lindbom&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2276935&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid18787642-68"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18787642_68-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSoehnleinKai-LarsenFrithiof2008" class="citation journal cs1">Soehnlein O, Kai-Larsen Y, Frithiof R (October 2008). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2532980">"Neutrophil primary granule proteins HBP and HNP1-3 boost bacterial phagocytosis by human and murine macrophages"</a>. <i>J. Clin. Invest</i>. <b>118</b> (10): 3491–502. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1172%2FJCI35740">10.1172/JCI35740</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2532980">2532980</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18787642">18787642</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Clin.+Invest.&rft.atitle=Neutrophil+primary+granule+proteins+HBP+and+HNP1-3+boost+bacterial+phagocytosis+by+human+and+murine+macrophages&rft.volume=118&rft.issue=10&rft.pages=3491-502&rft.date=2008-10&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2532980%23id-name%3DPMC&rft_id=info%3Apmid%2F18787642&rft_id=info%3Adoi%2F10.1172%2FJCI35740&rft.aulast=Soehnlein&rft.aufirst=O&rft.au=Kai-Larsen%2C+Y&rft.au=Frithiof%2C+R&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2532980&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid28990587-69"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid28990587_69-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFPapayannopoulos2018" class="citation journal cs1">Papayannopoulos V (February 2018). "Neutrophil extracellular traps in immunity and disease". <i>Nature Reviews. Immunology</i>. <b>18</b> (2): 134–147. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fnri.2017.105">10.1038/nri.2017.105</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/28990587">28990587</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:25067858">25067858</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Nature+Reviews.+Immunology&rft.atitle=Neutrophil+extracellular+traps+in+immunity+and+disease&rft.volume=18&rft.issue=2&rft.pages=134-147&rft.date=2018-02&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A25067858%23id-name%3DS2CID&rft_id=info%3Apmid%2F28990587&rft_id=info%3Adoi%2F10.1038%2Fnri.2017.105&rft.aulast=Papayannopoulos&rft.aufirst=V&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-Steinman-70"><span class="mw-cite-backlink"><b><a href="#cite_ref-Steinman_70-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSteinman_RM,_Cohn_ZACohn1973" class="citation journal cs1">Steinman RM, Cohn ZA; Cohn (1973). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2139237">"Identification of a novel cell type in peripheral lymphoid organs of mice. I. Morphology, quantitation, tissue distribution"</a>. <i>J. Exp. Med</i>. <b>137</b> (5): 1142–62. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1084%2Fjem.137.5.1142">10.1084/jem.137.5.1142</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2139237">2139237</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/4573839">4573839</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Exp.+Med.&rft.atitle=Identification+of+a+novel+cell+type+in+peripheral+lymphoid+organs+of+mice.+I.+Morphology%2C+quantitation%2C+tissue+distribution&rft.volume=137&rft.issue=5&rft.pages=1142-62&rft.date=1973&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2139237%23id-name%3DPMC&rft_id=info%3Apmid%2F4573839&rft_id=info%3Adoi%2F10.1084%2Fjem.137.5.1142&rft.au=Steinman+RM%2C+Cohn+ZA&rft.au=Cohn&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2139237&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-rock-71"><span class="mw-cite-backlink">^ <a href="#cite_ref-rock_71-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-rock_71-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSteinman" class="citation web cs1">Steinman, Ralph. <a rel="nofollow" class="external text" href="http://www.rockefeller.edu/labheads/steinman/steinman-lab.php">"Dendritic Cells"</a>. The Rockefeller University<span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=unknown&rft.btitle=Dendritic+Cells&rft.pub=The+Rockefeller+University&rft.aulast=Steinman&rft.aufirst=Ralph&rft_id=http%3A%2F%2Fwww.rockefeller.edu%2Flabheads%2Fsteinman%2Fsteinman-lab.php&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-antigen-72"><span class="mw-cite-backlink"><b><a href="#cite_ref-antigen_72-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFGuermonprez_P,_Valladeau_J,_Zitvogel_L,_Théry_C,_Amigorena_SValladeauZitvogelThéry2002" class="citation journal cs1">Guermonprez P, Valladeau J, Zitvogel L, Théry C, Amigorena S; Valladeau; Zitvogel; Théry; Amigorena (2002). "Antigen presentation and T cell stimulation by dendritic cells". <i>Annu. Rev. Immunol</i>. <b>20</b>: 621–67. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1146%2Fannurev.immunol.20.100301.064828">10.1146/annurev.immunol.20.100301.064828</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11861614">11861614</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Annu.+Rev.+Immunol.&rft.atitle=Antigen+presentation+and+T+cell+stimulation+by+dendritic+cells&rft.volume=20&rft.pages=621-67&rft.date=2002&rft_id=info%3Adoi%2F10.1146%2Fannurev.immunol.20.100301.064828&rft_id=info%3Apmid%2F11861614&rft.au=Guermonprez+P%2C+Valladeau+J%2C+Zitvogel+L%2C+Th%C3%A9ry+C%2C+Amigorena+S&rft.au=Valladeau&rft.au=Zitvogel&rft.au=Th%C3%A9ry&rft.au=Amigorena&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-73"><span class="mw-cite-backlink"><b><a href="#cite_ref-73">^</a></b></span> <span class="reference-text"><a href="#CITEREFHoffbrandPettitMoss2005">Hoffbrand, Pettit & Moss 2005</a>, p. 134</span>
</li>
<li id="cite_note-74"><span class="mw-cite-backlink"><b><a href="#cite_ref-74">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSallusto_F,_Lanzavecchia_ALanzavecchia2002" class="citation journal cs1 cs1-prop-long-vol">Sallusto F, Lanzavecchia A; Lanzavecchia (2002). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3240143">"The instructive role of dendritic cells on T-cell responses"</a>. <i>Arthritis Res</i>. 4 Suppl 3 (Suppl 3): S127–32. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1186%2Far567">10.1186/ar567</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3240143">3240143</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/12110131">12110131</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Arthritis+Res.&rft.atitle=The+instructive+role+of+dendritic+cells+on+T-cell+responses&rft.volume=4+Suppl+3&rft.issue=Suppl+3&rft.pages=S127-32&rft.date=2002&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3240143%23id-name%3DPMC&rft_id=info%3Apmid%2F12110131&rft_id=info%3Adoi%2F10.1186%2Far567&rft.au=Sallusto+F%2C+Lanzavecchia+A&rft.au=Lanzavecchia&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3240143&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-75"><span class="mw-cite-backlink"><b><a href="#cite_ref-75">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, pp. 45–46</span>
</li>
<li id="cite_note-pmid19672091-76"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid19672091_76-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFNovak_N,_Bieber_T,_Peng_WMBieberPeng2010" class="citation journal cs1">Novak N, Bieber T, Peng WM; Bieber; Peng (2010). <a rel="nofollow" class="external text" href="https://www.karger.com/Article/PDF/000232565">"The immunoglobulin E-Toll-like receptor network"</a>. <i>International Archives of Allergy and Immunology</i>. <b>151</b> (1): 1–7. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1159%2F000232565">10.1159/000232565</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/19672091">19672091</a><span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=International+Archives+of+Allergy+and+Immunology&rft.atitle=The+immunoglobulin+E-Toll-like+receptor+network&rft.volume=151&rft.issue=1&rft.pages=1-7&rft.date=2010&rft_id=info%3Adoi%2F10.1159%2F000232565&rft_id=info%3Apmid%2F19672091&rft.au=Novak+N%2C+Bieber+T%2C+Peng+WM&rft.au=Bieber&rft.au=Peng&rft_id=https%3A%2F%2Fwww.karger.com%2FArticle%2FPDF%2F000232565&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid18936782-77"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18936782_77-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFKalesnikoff_J,_Galli_SJGalli2008" class="citation journal cs1">Kalesnikoff J, Galli SJ; Galli (November 2008). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2856637">"New developments in mast cell biology"</a>. <i>Nature Immunology</i>. <b>9</b> (11): 1215–23. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fni.f.216">10.1038/ni.f.216</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2856637">2856637</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18936782">18936782</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Nature+Immunology&rft.atitle=New+developments+in+mast+cell+biology&rft.volume=9&rft.issue=11&rft.pages=1215-23&rft.date=2008-11&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2856637%23id-name%3DPMC&rft_id=info%3Apmid%2F18936782&rft_id=info%3Adoi%2F10.1038%2Fni.f.216&rft.au=Kalesnikoff+J%2C+Galli+SJ&rft.au=Galli&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2856637&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-mast-78"><span class="mw-cite-backlink">^ <a href="#cite_ref-mast_78-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-mast_78-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFMalaviya_R,_Abraham_SNAbraham2001" class="citation journal cs1">Malaviya R, Abraham SN; Abraham (February 2001). "Mast cell modulation of immune responses to bacteria". <i>Immunol. Rev</i>. <b>179</b>: 16–24. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1034%2Fj.1600-065X.2001.790102.x">10.1034/j.1600-065X.2001.790102.x</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11292019">11292019</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:23115222">23115222</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Immunol.+Rev.&rft.atitle=Mast+cell+modulation+of+immune+responses+to+bacteria&rft.volume=179&rft.pages=16-24&rft.date=2001-02&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A23115222%23id-name%3DS2CID&rft_id=info%3Apmid%2F11292019&rft_id=info%3Adoi%2F10.1034%2Fj.1600-065X.2001.790102.x&rft.au=Malaviya+R%2C+Abraham+SN&rft.au=Abraham&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid8790416-79"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid8790416_79-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFConnell_I,_Agace_W,_Klemm_P,_Schembri_M,_Mărild_S,_Svanborg_CAgaceKlemmSchembri1996" class="citation journal cs1">Connell I, Agace W, Klemm P, Schembri M, Mărild S, Svanborg C; Agace; Klemm; Schembri; Mărild; Svanborg (September 1996). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC38514">"Type 1 fimbrial expression enhances <i>Escherichia coli</i> virulence for the urinary tract"</a>. <i>Proc. Natl. Acad. Sci. U.S.A</i>. <b>93</b> (18): 9827–32. <a href="/enwiki/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/1996PNAS...93.9827C">1996PNAS...93.9827C</a>. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1073%2Fpnas.93.18.9827">10.1073/pnas.93.18.9827</a></span>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC38514">38514</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/8790416">8790416</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Proc.+Natl.+Acad.+Sci.+U.S.A.&rft.atitle=Type+1+fimbrial+expression+enhances+Escherichia+coli+virulence+for+the+urinary+tract&rft.volume=93&rft.issue=18&rft.pages=9827-32&rft.date=1996-09&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC38514%23id-name%3DPMC&rft_id=info%3Apmid%2F8790416&rft_id=info%3Adoi%2F10.1073%2Fpnas.93.18.9827&rft_id=info%3Abibcode%2F1996PNAS...93.9827C&rft.au=Connell+I%2C+Agace+W%2C+Klemm+P%2C+Schembri+M%2C+M%C4%83rild+S%2C+Svanborg+C&rft.au=Agace&rft.au=Klemm&rft.au=Schembri&rft.au=M%C4%83rild&rft.au=Svanborg&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC38514&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid8568252-80"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid8568252_80-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFMalaviya_R,_Twesten_NJ,_Ross_EA,_Abraham_SN,_Pfeifer_JDTwestenRossAbraham1996" class="citation journal cs1">Malaviya R, Twesten NJ, Ross EA, Abraham SN, Pfeifer JD; Twesten; Ross; Abraham; Pfeifer (February 1996). <a rel="nofollow" class="external text" href="http://www.jimmunol.org/cgi/pmidlookup?view=long&pmid=8568252">"Mast cells process bacterial Ags through a phagocytic route for class I MHC presentation to T cells"</a>. <i>J. Immunol</i>. <b>156</b> (4): 1490–96. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/8568252">8568252</a><span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Immunol.&rft.atitle=Mast+cells+process+bacterial+Ags+through+a+phagocytic+route+for+class+I+MHC+presentation+to+T+cells&rft.volume=156&rft.issue=4&rft.pages=1490-96&rft.date=1996-02&rft_id=info%3Apmid%2F8568252&rft.au=Malaviya+R%2C+Twesten+NJ%2C+Ross+EA%2C+Abraham+SN%2C+Pfeifer+JD&rft.au=Twesten&rft.au=Ross&rft.au=Abraham&rft.au=Pfeifer&rft_id=http%3A%2F%2Fwww.jimmunol.org%2Fcgi%2Fpmidlookup%3Fview%3Dlong%26pmid%3D8568252&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid11424870-81"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid11424870_81-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFTaylor_ML,_Metcalfe_DDMetcalfe2001" class="citation journal cs1">Taylor ML, Metcalfe DD; Metcalfe (2001). "Mast cells in allergy and host defense". <i>Allergy Asthma Proc</i>. <b>22</b> (3): 115–19. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.2500%2F108854101778148764">10.2500/108854101778148764</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11424870">11424870</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Allergy+Asthma+Proc&rft.atitle=Mast+cells+in+allergy+and+host+defense&rft.volume=22&rft.issue=3&rft.pages=115-19&rft.date=2001&rft_id=info%3Adoi%2F10.2500%2F108854101778148764&rft_id=info%3Apmid%2F11424870&rft.au=Taylor+ML%2C+Metcalfe+DD&rft.au=Metcalfe&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid22577358-82"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid22577358_82-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFUrbSheppard2012" class="citation journal cs1">Urb M, Sheppard DC (2012). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3343118">"The role of mast cells in the defence against pathogens"</a>. <i>PLOS Pathogens</i>. <b>8</b> (4): e1002619. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1371%2Fjournal.ppat.1002619">10.1371/journal.ppat.1002619</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3343118">3343118</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/22577358">22577358</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=PLOS+Pathogens&rft.atitle=The+role+of+mast+cells+in+the+defence+against+pathogens&rft.volume=8&rft.issue=4&rft.pages=e1002619&rft.date=2012&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3343118%23id-name%3DPMC&rft_id=info%3Apmid%2F22577358&rft_id=info%3Adoi%2F10.1371%2Fjournal.ppat.1002619&rft.aulast=Urb&rft.aufirst=M&rft.au=Sheppard%2C+DC&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3343118&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-superman-83"><span class="mw-cite-backlink">^ <a href="#cite_ref-superman_83-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-superman_83-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><a href="#CITEREFPaolettiNotarioRicevuti1997">Paoletti, Notario & Ricevuti 1997</a>, p. 427</span>
</li>
<li id="cite_note-pmid18451871-84"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18451871_84-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFBirge_RB,_Ucker_DSUcker2008" class="citation journal cs1">Birge RB, Ucker DS; Ucker (July 2008). <a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fcdd.2008.58">"Innate apoptotic immunity: the calming touch of death"</a>. <i>Cell Death Differ</i>. <b>15</b> (7): 1096–1102. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fcdd.2008.58">10.1038/cdd.2008.58</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18451871">18451871</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Cell+Death+Differ.&rft.atitle=Innate+apoptotic+immunity%3A+the+calming+touch+of+death&rft.volume=15&rft.issue=7&rft.pages=1096-1102&rft.date=2008-07&rft_id=info%3Adoi%2F10.1038%2Fcdd.2008.58&rft_id=info%3Apmid%2F18451871&rft.au=Birge+RB%2C+Ucker+DS&rft.au=Ucker&rft_id=%2F%2Fdoi.org%2F10.1038%252Fcdd.2008.58&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid11083817-85"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid11083817_85-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFCouzinet_S,_Cejas_E,_Schittny_J,_Deplazes_P,_Weber_R,_Zimmerli_SCejasSchittnyDeplazes2000" class="citation journal cs1">Couzinet S, Cejas E, Schittny J, Deplazes P, Weber R, Zimmerli S; Cejas; Schittny; Deplazes; Weber; Zimmerli (December 2000). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC97802">"Phagocytic uptake of <i>Encephalitozoon cuniculi</i> by nonprofessional phagocytes"</a>. <i>Infect. Immun</i>. <b>68</b> (12): 6939–45. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1128%2FIAI.68.12.6939-6945.2000">10.1128/IAI.68.12.6939-6945.2000</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC97802">97802</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11083817">11083817</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Infect.+Immun.&rft.atitle=Phagocytic+uptake+of+Encephalitozoon+cuniculi+by+nonprofessional+phagocytes&rft.volume=68&rft.issue=12&rft.pages=6939-45&rft.date=2000-12&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC97802%23id-name%3DPMC&rft_id=info%3Apmid%2F11083817&rft_id=info%3Adoi%2F10.1128%2FIAI.68.12.6939-6945.2000&rft.au=Couzinet+S%2C+Cejas+E%2C+Schittny+J%2C+Deplazes+P%2C+Weber+R%2C+Zimmerli+S&rft.au=Cejas&rft.au=Schittny&rft.au=Deplazes&rft.au=Weber&rft.au=Zimmerli&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC97802&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-86"><span class="mw-cite-backlink"><b><a href="#cite_ref-86">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSegal_G,_Lee_W,_Arora_PD,_McKee_M,_Downey_G,_McCulloch_CALeeAroraMcKee2001" class="citation journal cs1">Segal G, Lee W, Arora PD, McKee M, Downey G, McCulloch CA; Lee; Arora; McKee; Downey; McCulloch (January 2001). "Involvement of actin filaments and integrins in the binding step in collagen phagocytosis by human fibroblasts". <i>Journal of Cell Science</i>. <b>114</b> (Pt 1): 119–129. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1242%2Fjcs.114.1.119">10.1242/jcs.114.1.119</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11112696">11112696</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Journal+of+Cell+Science&rft.atitle=Involvement+of+actin+filaments+and+integrins+in+the+binding+step+in+collagen+phagocytosis+by+human+fibroblasts&rft.volume=114&rft.issue=Pt+1&rft.pages=119-129&rft.date=2001-01&rft_id=info%3Adoi%2F10.1242%2Fjcs.114.1.119&rft_id=info%3Apmid%2F11112696&rft.au=Segal+G%2C+Lee+W%2C+Arora+PD%2C+McKee+M%2C+Downey+G%2C+McCulloch+CA&rft.au=Lee&rft.au=Arora&rft.au=McKee&rft.au=Downey&rft.au=McCulloch&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-something-87"><span class="mw-cite-backlink"><b><a href="#cite_ref-something_87-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>something</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-pmid14732160-88"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid14732160_88-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFRabinovitch_M1995" class="citation journal cs1">Rabinovitch M (March 1995). "Professional and non-professional phagocytes: an introduction". <i>Trends Cell Biol</i>. <b>5</b> (3): 85–87. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS0962-8924%2800%2988955-2">10.1016/S0962-8924(00)88955-2</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/14732160">14732160</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Trends+Cell+Biol.&rft.atitle=Professional+and+non-professional+phagocytes%3A+an+introduction&rft.volume=5&rft.issue=3&rft.pages=85-87&rft.date=1995-03&rft_id=info%3Adoi%2F10.1016%2FS0962-8924%2800%2988955-2&rft_id=info%3Apmid%2F14732160&rft.au=Rabinovitch+M&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid29321780-89"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid29321780_89-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFLinLoré2017" class="citation journal cs1">Lin A, Loré K (2017). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC5732227">"Granulocytes: New Members of the Antigen-Presenting Cell Family"</a>. <i>Frontiers in Immunology</i>. <b>8</b>: 1781. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.3389%2Ffimmu.2017.01781">10.3389/fimmu.2017.01781</a></span>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC5732227">5732227</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/29321780">29321780</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Frontiers+in+Immunology&rft.atitle=Granulocytes%3A+New+Members+of+the+Antigen-Presenting+Cell+Family&rft.volume=8&rft.pages=1781&rft.date=2017&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC5732227%23id-name%3DPMC&rft_id=info%3Apmid%2F29321780&rft_id=info%3Adoi%2F10.3389%2Ffimmu.2017.01781&rft.aulast=Lin&rft.aufirst=A&rft.au=Lor%C3%A9%2C+K&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC5732227&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-chicken-90"><span class="mw-cite-backlink">^ <a href="#cite_ref-chicken_90-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-chicken_90-1"><sup><i><b>b</b></i></sup></a> <a href="#cite_ref-chicken_90-2"><sup><i><b>c</b></i></sup></a> <a href="#cite_ref-chicken_90-3"><sup><i><b>d</b></i></sup></a> <a href="#cite_ref-chicken_90-4"><sup><i><b>e</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFTodar" class="citation web cs1">Todar, Kenneth. <a rel="nofollow" class="external text" href="http://textbookofbacteriology.net/antiphago.html">"Mechanisms of Bacterial Pathogenicity: Bacterial Defense Against Phagocytes"</a>. 2008<span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=unknown&rft.btitle=Mechanisms+of+Bacterial+Pathogenicity%3A+Bacterial+Defense+Against+Phagocytes&rft.pub=2008&rft.aulast=Todar&rft.aufirst=Kenneth&rft_id=http%3A%2F%2Ftextbookofbacteriology.net%2Fantiphago.html&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-91"><span class="mw-cite-backlink"><b><a href="#cite_ref-91">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFAlexander_J,_Satoskar_AR,_Russell_DGSatoskarRussell1999" class="citation journal cs1">Alexander J, Satoskar AR, Russell DG; Satoskar; Russell (September 1999). <a rel="nofollow" class="external text" href="http://jcs.biologists.org/cgi/pmidlookup?view=long&pmid=10462516">"Leishmania species: models of intracellular parasitism"</a>. <i>J. Cell Sci</i>. <b>112</b> (18): 2993–3002. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1242%2Fjcs.112.18.2993">10.1242/jcs.112.18.2993</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/10462516">10462516</a><span class="reference-accessdate">. Retrieved <span class="nowrap">December 19,</span> 2014</span>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Cell+Sci.&rft.atitle=Leishmania+species%3A+models+of+intracellular+parasitism&rft.volume=112&rft.issue=18&rft.pages=2993-3002&rft.date=1999-09&rft_id=info%3Adoi%2F10.1242%2Fjcs.112.18.2993&rft_id=info%3Apmid%2F10462516&rft.au=Alexander+J%2C+Satoskar+AR%2C+Russell+DG&rft.au=Satoskar&rft.au=Russell&rft_id=http%3A%2F%2Fjcs.biologists.org%2Fcgi%2Fpmidlookup%3Fview%3Dlong%26pmid%3D10462516&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid11973157-92"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid11973157_92-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFCelli_J,_Finlay_BBFinlay2002" class="citation journal cs1">Celli J, Finlay BB; Finlay (May 2002). "Bacterial avoidance of phagocytosis". <i>Trends Microbiol</i>. <b>10</b> (5): 232–37. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS0966-842X%2802%2902343-0">10.1016/S0966-842X(02)02343-0</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11973157">11973157</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Trends+Microbiol.&rft.atitle=Bacterial+avoidance+of+phagocytosis&rft.volume=10&rft.issue=5&rft.pages=232-37&rft.date=2002-05&rft_id=info%3Adoi%2F10.1016%2FS0966-842X%2802%2902343-0&rft_id=info%3Apmid%2F11973157&rft.au=Celli+J%2C+Finlay+BB&rft.au=Finlay&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid15992798-93"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid15992798_93-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFValenick_LV,_Hsia_HC,_Schwarzbauer_JEHsiaSchwarzbauer2005" class="citation journal cs1">Valenick LV, Hsia HC, Schwarzbauer JE; Hsia; Schwarzbauer (September 2005). "Fibronectin fragmentation promotes alpha4beta1 integrin-mediated contraction of a fibrin-fibronectin provisional matrix". <i>Experimental Cell Research</i>. <b>309</b> (1): 48–55. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.yexcr.2005.05.024">10.1016/j.yexcr.2005.05.024</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/15992798">15992798</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Experimental+Cell+Research&rft.atitle=Fibronectin+fragmentation+promotes+alpha4beta1+integrin-mediated+contraction+of+a+fibrin-fibronectin+provisional+matrix&rft.volume=309&rft.issue=1&rft.pages=48-55&rft.date=2005-09&rft_id=info%3Adoi%2F10.1016%2Fj.yexcr.2005.05.024&rft_id=info%3Apmid%2F15992798&rft.au=Valenick+LV%2C+Hsia+HC%2C+Schwarzbauer+JE&rft.au=Hsia&rft.au=Schwarzbauer&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid10417134-94"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid10417134_94-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFBurns_SM,_Hull_SIHull1999" class="citation journal cs1">Burns SM, Hull SI; Hull (August 1999). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC96650">"Loss of resistance to ingestion and phagocytic killing by O(-) and K(-) mutants of a uropathogenic <i>Escherichia coli</i> O75:K5 strain"</a>. <i>Infect. Immun</i>. <b>67</b> (8): 3757–62. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1128%2FIAI.67.8.3757-3762.1999">10.1128/IAI.67.8.3757-3762.1999</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC96650">96650</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/10417134">10417134</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Infect.+Immun.&rft.atitle=Loss+of+resistance+to+ingestion+and+phagocytic+killing+by+O%28-%29+and+K%28-%29+mutants+of+a+uropathogenic+Escherichia+coli+O75%3AK5+strain&rft.volume=67&rft.issue=8&rft.pages=3757-62&rft.date=1999-08&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC96650%23id-name%3DPMC&rft_id=info%3Apmid%2F10417134&rft_id=info%3Adoi%2F10.1128%2FIAI.67.8.3757-3762.1999&rft.au=Burns+SM%2C+Hull+SI&rft.au=Hull&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC96650&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid15501828-95"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid15501828_95-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFVuongKocianovaVoyich2004" class="citation journal cs1">Vuong C, Kocianova S, Voyich JM (December 2004). <a rel="nofollow" class="external text" href="https://doi.org/10.1074%2Fjbc.M411374200">"A crucial role for exopolysaccharide modification in bacterial biofilm formation, immune evasion, and virulence"</a>. <i>J. Biol. Chem</i>. <b>279</b> (52): 54881–86. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1074%2Fjbc.M411374200">10.1074/jbc.M411374200</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/15501828">15501828</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Biol.+Chem.&rft.atitle=A+crucial+role+for+exopolysaccharide+modification+in+bacterial+biofilm+formation%2C+immune+evasion%2C+and+virulence&rft.volume=279&rft.issue=52&rft.pages=54881-86&rft.date=2004-12&rft_id=info%3Adoi%2F10.1074%2Fjbc.M411374200&rft_id=info%3Apmid%2F15501828&rft.aulast=Vuong&rft.aufirst=C&rft.au=Kocianova%2C+S&rft.au=Voyich%2C+JM&rft_id=%2F%2Fdoi.org%2F10.1074%252Fjbc.M411374200&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid19047408-96"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid19047408_96-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFMelin_M,_Jarva_H,_Siira_L,_Meri_S,_Käyhty_H,_Väkeväinen_MJarvaSiiraMeri2009" class="citation journal cs1">Melin M, Jarva H, Siira L, Meri S, Käyhty H, Väkeväinen M; Jarva; Siira; Meri; Käyhty; Väkeväinen (February 2009). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2632042">"<i>Streptococcus pneumoniae</i> capsular serotype 19F is more resistant to C3 deposition and less sensitive to opsonophagocytosis than serotype 6B"</a>. <i>Infect. Immun</i>. <b>77</b> (2): 676–84. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1128%2FIAI.01186-08">10.1128/IAI.01186-08</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC2632042">2632042</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/19047408">19047408</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Infect.+Immun.&rft.atitle=Streptococcus+pneumoniae+capsular+serotype+19F+is+more+resistant+to+C3+deposition+and+less+sensitive+to+opsonophagocytosis+than+serotype+6B&rft.volume=77&rft.issue=2&rft.pages=676-84&rft.date=2009-02&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2632042%23id-name%3DPMC&rft_id=info%3Apmid%2F19047408&rft_id=info%3Adoi%2F10.1128%2FIAI.01186-08&rft.au=Melin+M%2C+Jarva+H%2C+Siira+L%2C+Meri+S%2C+K%C3%A4yhty+H%2C+V%C3%A4kev%C3%A4inen+M&rft.au=Jarva&rft.au=Siira&rft.au=Meri&rft.au=K%C3%A4yhty&rft.au=V%C3%A4kev%C3%A4inen&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC2632042&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid16322743-97"><span class="mw-cite-backlink">^ <a href="#cite_ref-pmid16322743_97-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-pmid16322743_97-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFFoster_TJ2005" class="citation journal cs1">Foster TJ (December 2005). "Immune evasion by staphylococci". <i>Nat. Rev. Microbiol</i>. <b>3</b> (12): 948–58. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1038%2Fnrmicro1289">10.1038/nrmicro1289</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/16322743">16322743</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:205496221">205496221</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Nat.+Rev.+Microbiol.&rft.atitle=Immune+evasion+by+staphylococci&rft.volume=3&rft.issue=12&rft.pages=948-58&rft.date=2005-12&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A205496221%23id-name%3DS2CID&rft_id=info%3Apmid%2F16322743&rft_id=info%3Adoi%2F10.1038%2Fnrmicro1289&rft.au=Foster+TJ&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid11890550-98"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid11890550_98-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFFällmanDeleuilMcGee2002" class="citation journal cs1">Fällman M, Deleuil F, McGee K (February 2002). "Resistance to phagocytosis by Yersinia". <i>International Journal of Medical Microbiology</i>. <b>291</b> (6–7): 501–9. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1078%2F1438-4221-00159">10.1078/1438-4221-00159</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11890550">11890550</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=International+Journal+of+Medical+Microbiology&rft.atitle=Resistance+to+phagocytosis+by+Yersinia&rft.volume=291&rft.issue=6%E2%80%937&rft.pages=501-9&rft.date=2002-02&rft_id=info%3Adoi%2F10.1078%2F1438-4221-00159&rft_id=info%3Apmid%2F11890550&rft.aulast=F%C3%A4llman&rft.aufirst=M&rft.au=Deleuil%2C+F&rft.au=McGee%2C+K&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid11708894-99"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid11708894_99-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSansonetti_P2001" class="citation journal cs1">Sansonetti P (December 2001). "Phagocytosis of bacterial pathogens: implications in the host response". <i>Semin. Immunol</i>. <b>13</b> (6): 381–90. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1006%2Fsmim.2001.0335">10.1006/smim.2001.0335</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11708894">11708894</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Semin.+Immunol.&rft.atitle=Phagocytosis+of+bacterial+pathogens%3A+implications+in+the+host+response&rft.volume=13&rft.issue=6&rft.pages=381-90&rft.date=2001-12&rft_id=info%3Adoi%2F10.1006%2Fsmim.2001.0335&rft_id=info%3Apmid%2F11708894&rft.au=Sansonetti+P&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid10064587-100"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid10064587_100-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFDersch_P,_Isberg_RRIsberg1999" class="citation journal cs1">Dersch P, Isberg RR; Isberg (March 1999). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC1171211">"A region of the <i>Yersinia pseudotuberculosis</i> invasin protein enhances integrin-mediated uptake into mammalian cells and promotes self-association"</a>. <i>EMBO J</i>. <b>18</b> (5): 1199–1213. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1093%2Femboj%2F18.5.1199">10.1093/emboj/18.5.1199</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC1171211">1171211</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/10064587">10064587</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=EMBO+J.&rft.atitle=A+region+of+the+Yersinia+pseudotuberculosis+invasin+protein+enhances+integrin-mediated+uptake+into+mammalian+cells+and+promotes+self-association&rft.volume=18&rft.issue=5&rft.pages=1199-1213&rft.date=1999-03&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1171211%23id-name%3DPMC&rft_id=info%3Apmid%2F10064587&rft_id=info%3Adoi%2F10.1093%2Femboj%2F18.5.1199&rft.au=Dersch+P%2C+Isberg+RR&rft.au=Isberg&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1171211&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-101"><span class="mw-cite-backlink"><b><a href="#cite_ref-101">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFAntoine_JC,_Prina_E,_Lang_T,_Courret_NPrinaLangCourret1998" class="citation journal cs1">Antoine JC, Prina E, Lang T, Courret N; Prina; Lang; Courret (October 1998). "The biogenesis and properties of the parasitophorous vacuoles that harbour <i>Leishmania</i> in murine macrophages". <i>Trends Microbiol</i>. <b>6</b> (10): 392–401. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS0966-842X%2898%2901324-9">10.1016/S0966-842X(98)01324-9</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/9807783">9807783</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Trends+Microbiol.&rft.atitle=The+biogenesis+and+properties+of+the+parasitophorous+vacuoles+that+harbour+Leishmania+in+murine+macrophages&rft.volume=6&rft.issue=10&rft.pages=392-401&rft.date=1998-10&rft_id=info%3Adoi%2F10.1016%2FS0966-842X%2898%2901324-9&rft_id=info%3Apmid%2F9807783&rft.au=Antoine+JC%2C+Prina+E%2C+Lang+T%2C+Courret+N&rft.au=Prina&rft.au=Lang&rft.au=Courret&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid18607538-102"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid18607538_102-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFDas_D,_Saha_SS,_Bishayi_BSahaBishayi2008" class="citation journal cs1">Das D, Saha SS, Bishayi B; Saha; Bishayi (July 2008). "Intracellular survival of <i>Staphylococcus aureus</i>: correlating production of catalase and superoxide dismutase with levels of inflammatory cytokines". <i>Inflamm. Res</i>. <b>57</b> (7): 340–49. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1007%2Fs00011-007-7206-z">10.1007/s00011-007-7206-z</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18607538">18607538</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:22127111">22127111</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Inflamm.+Res.&rft.atitle=Intracellular+survival+of+Staphylococcus+aureus%3A+correlating+production+of+catalase+and+superoxide+dismutase+with+levels+of+inflammatory+cytokines&rft.volume=57&rft.issue=7&rft.pages=340-49&rft.date=2008-07&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A22127111%23id-name%3DS2CID&rft_id=info%3Apmid%2F18607538&rft_id=info%3Adoi%2F10.1007%2Fs00011-007-7206-z&rft.au=Das+D%2C+Saha+SS%2C+Bishayi+B&rft.au=Saha&rft.au=Bishayi&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid17517863-103"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid17517863_103-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFHara_H,_Kawamura_I,_Nomura_T,_Tominaga_T,_Tsuchiya_K,_Mitsuyama_MKawamuraNomuraTominaga2007" class="citation journal cs1">Hara H, Kawamura I, Nomura T, Tominaga T, Tsuchiya K, Mitsuyama M; Kawamura; Nomura; Tominaga; Tsuchiya; Mitsuyama (August 2007). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC1951982">"Cytolysin-dependent escape of the bacterium from the phagosome is required but not sufficient for induction of the Th1 immune response against Listeria monocytogenes infection: distinct role of Listeriolysin O determined by cytolysin gene replacement"</a>. <i>Infect. Immun</i>. <b>75</b> (8): 3791–3801. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1128%2FIAI.01779-06">10.1128/IAI.01779-06</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC1951982">1951982</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17517863">17517863</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Infect.+Immun.&rft.atitle=Cytolysin-dependent+escape+of+the+bacterium+from+the+phagosome+is+required+but+not+sufficient+for+induction+of+the+Th1+immune+response+against+Listeria+monocytogenes+infection%3A+distinct+role+of+Listeriolysin+O+determined+by+cytolysin+gene+replacement&rft.volume=75&rft.issue=8&rft.pages=3791-3801&rft.date=2007-08&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1951982%23id-name%3DPMC&rft_id=info%3Apmid%2F17517863&rft_id=info%3Adoi%2F10.1128%2FIAI.01779-06&rft.au=Hara+H%2C+Kawamura+I%2C+Nomura+T%2C+Tominaga+T%2C+Tsuchiya+K%2C+Mitsuyama+M&rft.au=Kawamura&rft.au=Nomura&rft.au=Tominaga&rft.au=Tsuchiya&rft.au=Mitsuyama&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1951982&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid15819624-104"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid15819624_104-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFDatta_V,_Myskowski_SM,_Kwinn_LA,_Chiem_DN,_Varki_N,_Kansal_RG,_Kotb_M,_Nizet_VMyskowskiKwinnChiem2005" class="citation journal cs1">Datta V, Myskowski SM, Kwinn LA, Chiem DN, Varki N, Kansal RG, Kotb M, Nizet V; Myskowski; Kwinn; Chiem; Varki; Kansal; Kotb; Nizet (May 2005). <a rel="nofollow" class="external text" href="https://doi.org/10.1111%2Fj.1365-2958.2005.04583.x">"Mutational analysis of the group A streptococcal operon encoding streptolysin S and its virulence role in invasive infection"</a>. <i>Mol. Microbiol</i>. <b>56</b> (3): 681–95. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1111%2Fj.1365-2958.2005.04583.x">10.1111/j.1365-2958.2005.04583.x</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/15819624">15819624</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:14748436">14748436</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Mol.+Microbiol.&rft.atitle=Mutational+analysis+of+the+group+A+streptococcal+operon+encoding+streptolysin+S+and+its+virulence+role+in+invasive+infection&rft.volume=56&rft.issue=3&rft.pages=681-95&rft.date=2005-05&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A14748436%23id-name%3DS2CID&rft_id=info%3Apmid%2F15819624&rft_id=info%3Adoi%2F10.1111%2Fj.1365-2958.2005.04583.x&rft.au=Datta+V%2C+Myskowski+SM%2C+Kwinn+LA%2C+Chiem+DN%2C+Varki+N%2C+Kansal+RG%2C+Kotb+M%2C+Nizet+V&rft.au=Myskowski&rft.au=Kwinn&rft.au=Chiem&rft.au=Varki&rft.au=Kansal&rft.au=Kotb&rft.au=Nizet&rft_id=%2F%2Fdoi.org%2F10.1111%252Fj.1365-2958.2005.04583.x&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid16679003-105"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid16679003_105-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFIwatsuki_K,_Yamasaki_O,_Morizane_S,_Oono_TYamasakiMorizaneOono2006" class="citation journal cs1">Iwatsuki K, Yamasaki O, Morizane S, Oono T; Yamasaki; Morizane; Oono (June 2006). "Staphylococcal cutaneous infections: invasion, evasion and aggression". <i>J. Dermatol. Sci</i>. <b>42</b> (3): 203–14. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.jdermsci.2006.03.011">10.1016/j.jdermsci.2006.03.011</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/16679003">16679003</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=J.+Dermatol.+Sci.&rft.atitle=Staphylococcal+cutaneous+infections%3A+invasion%2C+evasion+and+aggression&rft.volume=42&rft.issue=3&rft.pages=203-14&rft.date=2006-06&rft_id=info%3Adoi%2F10.1016%2Fj.jdermsci.2006.03.011&rft_id=info%3Apmid%2F16679003&rft.au=Iwatsuki+K%2C+Yamasaki+O%2C+Morizane+S%2C+Oono+T&rft.au=Yamasaki&rft.au=Morizane&rft.au=Oono&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid15639739-106"><span class="mw-cite-backlink">^ <a href="#cite_ref-pmid15639739_106-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-pmid15639739_106-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFDenkers_EY,_Butcher_BAButcher2005" class="citation journal cs1">Denkers EY, Butcher BA; Butcher (January 2005). "Sabotage and exploitation in macrophages parasitized by intracellular protozoans". <i>Trends Parasitol</i>. <b>21</b> (1): 35–41. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.pt.2004.10.004">10.1016/j.pt.2004.10.004</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/15639739">15639739</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Trends+Parasitol.&rft.atitle=Sabotage+and+exploitation+in+macrophages+parasitized+by+intracellular+protozoans&rft.volume=21&rft.issue=1&rft.pages=35-41&rft.date=2005-01&rft_id=info%3Adoi%2F10.1016%2Fj.pt.2004.10.004&rft_id=info%3Apmid%2F15639739&rft.au=Denkers+EY%2C+Butcher+BA&rft.au=Butcher&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid16281989-107"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid16281989_107-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFGregory_DJ,_Olivier_MOlivier2005" class="citation journal cs1 cs1-prop-long-vol">Gregory DJ, Olivier M; Olivier (2005). "Subversion of host cell signalling by the protozoan parasite <i>Leishmania</i>". <i>Parasitology</i>. 130 Suppl: S27–35. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1017%2FS0031182005008139">10.1017/S0031182005008139</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/16281989">16281989</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:24696519">24696519</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Parasitology&rft.atitle=Subversion+of+host+cell+signalling+by+the+protozoan+parasite+Leishmania&rft.volume=130+Suppl&rft.pages=S27-35&rft.date=2005&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A24696519%23id-name%3DS2CID&rft_id=info%3Apmid%2F16281989&rft_id=info%3Adoi%2F10.1017%2FS0031182005008139&rft.au=Gregory+DJ%2C+Olivier+M&rft.au=Olivier&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-108"><span class="mw-cite-backlink"><b><a href="#cite_ref-108">^</a></b></span> <span class="reference-text">Paoletti pp. 426–30</span>
</li>
<li id="cite_note-pmid10430993-109"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid10430993_109-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFHeinzelmann_M,_Mercer-Jones_MA,_Passmore_JCMercer-JonesPassmore1999" class="citation journal cs1">Heinzelmann M, Mercer-Jones MA, Passmore JC; Mercer-Jones; Passmore (August 1999). "Neutrophils and renal failure". <i>Am. J. Kidney Dis</i>. <b>34</b> (2): 384–99. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS0272-6386%2899%2970375-6">10.1016/S0272-6386(99)70375-6</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/10430993">10430993</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Am.+J.+Kidney+Dis.&rft.atitle=Neutrophils+and+renal+failure&rft.volume=34&rft.issue=2&rft.pages=384-99&rft.date=1999-08&rft_id=info%3Adoi%2F10.1016%2FS0272-6386%2899%2970375-6&rft_id=info%3Apmid%2F10430993&rft.au=Heinzelmann+M%2C+Mercer-Jones+MA%2C+Passmore+JC&rft.au=Mercer-Jones&rft.au=Passmore&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid11373504-110"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid11373504_110-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFLee_WL,_Downey_GPDowney2001" class="citation journal cs1">Lee WL, Downey GP; Downey (February 2001). "Neutrophil activation and acute lung injury". <i>Curr Opin Crit Care</i>. <b>7</b> (1): 1–7. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1097%2F00075198-200102000-00001">10.1097/00075198-200102000-00001</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/11373504">11373504</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:24164360">24164360</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Curr+Opin+Crit+Care&rft.atitle=Neutrophil+activation+and+acute+lung+injury&rft.volume=7&rft.issue=1&rft.pages=1-7&rft.date=2001-02&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A24164360%23id-name%3DS2CID&rft_id=info%3Apmid%2F11373504&rft_id=info%3Adoi%2F10.1097%2F00075198-200102000-00001&rft.au=Lee+WL%2C+Downey+GP&rft.au=Downey&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid16319683-111"><span class="mw-cite-backlink">^ <a href="#cite_ref-pmid16319683_111-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-pmid16319683_111-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFMoraes_TJ,_Zurawska_JH,_Downey_GPZurawskaDowney2006" class="citation journal cs1">Moraes TJ, Zurawska JH, Downey GP; Zurawska; Downey (January 2006). "Neutrophil granule contents in the pathogenesis of lung injury". <i>Curr. Opin. Hematol</i>. <b>13</b> (1): 21–27. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1097%2F01.moh.0000190113.31027.d5">10.1097/01.moh.0000190113.31027.d5</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/16319683">16319683</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:29374195">29374195</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Curr.+Opin.+Hematol.&rft.atitle=Neutrophil+granule+contents+in+the+pathogenesis+of+lung+injury&rft.volume=13&rft.issue=1&rft.pages=21-27&rft.date=2006-01&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A29374195%23id-name%3DS2CID&rft_id=info%3Apmid%2F16319683&rft_id=info%3Adoi%2F10.1097%2F01.moh.0000190113.31027.d5&rft.au=Moraes+TJ%2C+Zurawska+JH%2C+Downey+GP&rft.au=Zurawska&rft.au=Downey&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid12682440-112"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid12682440_112-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFAbraham_E2003" class="citation journal cs1">Abraham E (April 2003). <a rel="nofollow" class="external text" href="https://semanticscholar.org/paper/33d1bbeddab0d02bbd37634dab1e745258500732">"Neutrophils and acute lung injury"</a>. <i>Crit. Care Med</i>. <b>31</b> (4 Suppl): S195–99. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1097%2F01.CCM.0000057843.47705.E8">10.1097/01.CCM.0000057843.47705.E8</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/12682440">12682440</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:4004607">4004607</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Crit.+Care+Med.&rft.atitle=Neutrophils+and+acute+lung+injury&rft.volume=31&rft.issue=4+Suppl&rft.pages=S195-99&rft.date=2003-04&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A4004607%23id-name%3DS2CID&rft_id=info%3Apmid%2F12682440&rft_id=info%3Adoi%2F10.1097%2F01.CCM.0000057843.47705.E8&rft.au=Abraham+E&rft_id=https%3A%2F%2Fsemanticscholar.org%2Fpaper%2F33d1bbeddab0d02bbd37634dab1e745258500732&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid9704069-113"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid9704069_113-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFRicevuti_G1997" class="citation journal cs1">Ricevuti G (December 1997). "Host tissue damage by phagocytes". <i>Ann. N. Y. Acad. Sci</i>. <b>832</b> (1): 426–48. <a href="/enwiki/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/1997NYASA.832..426R">1997NYASA.832..426R</a>. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1111%2Fj.1749-6632.1997.tb46269.x">10.1111/j.1749-6632.1997.tb46269.x</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/9704069">9704069</a>. <a href="/enwiki/wiki/S2CID_(identifier)" class="mw-redirect" title="S2CID (identifier)">S2CID</a> <a rel="nofollow" class="external text" href="https://api.semanticscholar.org/CorpusID:10318084">10318084</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Ann.+N.+Y.+Acad.+Sci.&rft.atitle=Host+tissue+damage+by+phagocytes&rft.volume=832&rft.issue=1&rft.pages=426-48&rft.date=1997-12&rft_id=info%3Adoi%2F10.1111%2Fj.1749-6632.1997.tb46269.x&rft_id=https%3A%2F%2Fapi.semanticscholar.org%2FCorpusID%3A10318084%23id-name%3DS2CID&rft_id=info%3Apmid%2F9704069&rft_id=info%3Abibcode%2F1997NYASA.832..426R&rft.au=Ricevuti+G&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid17135502-114"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid17135502_114-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFCharley_B,_Riffault_S,_Van_Reeth_KRiffaultVan_Reeth2006" class="citation journal cs1">Charley B, Riffault S, Van Reeth K; Riffault; Van Reeth (October 2006). <a rel="nofollow" class="external text" href="https://biblio.ugent.be/publication/369324">"Porcine innate and adaptative immune responses to influenza and coronavirus infections"</a>. <i>Ann. N. Y. Acad. Sci</i>. <b>1081</b> (1): 130–36. <a href="/enwiki/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/2006NYASA1081..130C">2006NYASA1081..130C</a>. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="https://doi.org/10.1196%2Fannals.1373.014">10.1196/annals.1373.014</a></span>. <a href="/enwiki/wiki/Hdl_(identifier)" class="mw-redirect" title="Hdl (identifier)">hdl</a>:<a rel="nofollow" class="external text" href="/enwiki//hdl.handle.net/1854%2FLU-369324">1854/LU-369324</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC7168046">7168046</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17135502">17135502</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Ann.+N.+Y.+Acad.+Sci.&rft.atitle=Porcine+innate+and+adaptative+immune+responses+to+influenza+and+coronavirus+infections&rft.volume=1081&rft.issue=1&rft.pages=130-36&rft.date=2006-10&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC7168046%23id-name%3DPMC&rft_id=info%3Abibcode%2F2006NYASA1081..130C&rft_id=info%3Apmid%2F17135502&rft_id=info%3Adoi%2F10.1196%2Fannals.1373.014&rft_id=info%3Ahdl%2F1854%2FLU-369324&rft.au=Charley+B%2C+Riffault+S%2C+Van+Reeth+K&rft.au=Riffault&rft.au=Van+Reeth&rft_id=https%3A%2F%2Fbiblio.ugent.be%2Fpublication%2F369324&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-115"><span class="mw-cite-backlink"><b><a href="#cite_ref-115">^</a></b></span> <span class="reference-text"><a href="#CITEREFSompayrac2019">Sompayrac 2019</a>, p. 2</span>
</li>
<li id="cite_note-pmid18550419-116"><span class="mw-cite-backlink">^ <a href="#cite_ref-pmid18550419_116-0"><sup><i><b>a</b></i></sup></a> <a href="#cite_ref-pmid18550419_116-1"><sup><i><b>b</b></i></sup></a></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFCosson_P,_Soldati_TSoldati2008" class="citation journal cs1">Cosson P, Soldati T; Soldati (June 2008). "Eat, kill or die: when amoeba meets bacteria". <i>Curr. Opin. Microbiol</i>. <b>11</b> (3): 271–76. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.mib.2008.05.005">10.1016/j.mib.2008.05.005</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/18550419">18550419</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Curr.+Opin.+Microbiol.&rft.atitle=Eat%2C+kill+or+die%3A+when+amoeba+meets+bacteria&rft.volume=11&rft.issue=3&rft.pages=271-76&rft.date=2008-06&rft_id=info%3Adoi%2F10.1016%2Fj.mib.2008.05.005&rft_id=info%3Apmid%2F18550419&rft.au=Cosson+P%2C+Soldati+T&rft.au=Soldati&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></span>
</li>
<li id="cite_note-pmid19081545-117"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid19081545_117-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFBozzaro_S,_Bucci_C,_Steinert_MBucciSteinert2008" class="citation book cs1">Bozzaro S, Bucci C, Steinert M; Bucci; Steinert (2008). <i>Phagocytosis and host-pathogen interactions in Dictyostelium with a look at macrophages</i>. <i>Int Rev Cell Mol Biol</i>. International Review of Cell and Molecular Biology. Vol. 271. pp. 253–300. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2FS1937-6448%2808%2901206-9">10.1016/S1937-6448(08)01206-9</a>. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/9780123747280" title="Special:BookSources/9780123747280"><bdi>9780123747280</bdi></a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/19081545">19081545</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Phagocytosis+and+host-pathogen+interactions+in+Dictyostelium+with+a+look+at+macrophages&rft.series=International+Review+of+Cell+and+Molecular+Biology&rft.pages=253-300&rft.date=2008&rft_id=info%3Apmid%2F19081545&rft_id=info%3Adoi%2F10.1016%2FS1937-6448%2808%2901206-9&rft.isbn=9780123747280&rft.au=Bozzaro+S%2C+Bucci+C%2C+Steinert+M&rft.au=Bucci&rft.au=Steinert&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_book" title="Template:Cite book">cite book</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-pmid17673666-118"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid17673666_118-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFChen_G,_Zhuchenko_O,_Kuspa_AZhuchenkoKuspa2007" class="citation journal cs1">Chen G, Zhuchenko O, Kuspa A; Zhuchenko; Kuspa (August 2007). <a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3291017">"Immune-like phagocyte activity in the social amoeba"</a>. <i>Science</i>. <b>317</b> (5838): 678–81. <a href="/enwiki/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/2007Sci...317..678C">2007Sci...317..678C</a>. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1126%2Fscience.1143991">10.1126/science.1143991</a>. <a href="/enwiki/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <span class="cs1-lock-free" title="Freely accessible"><a rel="nofollow" class="external text" href="/enwiki//www.ncbi.nlm.nih.gov/pmc/articles/PMC3291017">3291017</a></span>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/17673666">17673666</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Immune-like+phagocyte+activity+in+the+social+amoeba&rft.volume=317&rft.issue=5838&rft.pages=678-81&rft.date=2007-08&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3291017%23id-name%3DPMC&rft_id=info%3Apmid%2F17673666&rft_id=info%3Adoi%2F10.1126%2Fscience.1143991&rft_id=info%3Abibcode%2F2007Sci...317..678C&rft.au=Chen+G%2C+Zhuchenko+O%2C+Kuspa+A&rft.au=Zhuchenko&rft.au=Kuspa&rft_id=%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3291017&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-Delves250-119"><span class="mw-cite-backlink"><b><a href="#cite_ref-Delves250_119-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>Delves250</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
<li id="cite_note-120"><span class="mw-cite-backlink"><b><a href="#cite_ref-120">^</a></b></span> <span class="reference-text"><a href="#CITEREFDelvesMartinBurtonRoit2006">Delves et al. 2006</a>, pp. 251–252</span>
</li>
<li id="cite_note-pmid19063916-121"><span class="mw-cite-backlink"><b><a href="#cite_ref-pmid19063916_121-0">^</a></b></span> <span class="reference-text"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFHanington_PC,_Tam_J,_Katzenback_BA,_Hitchen_SJ,_Barreda_DR,_Belosevic_MTamKatzenbackHitchen2009" class="citation journal cs1">Hanington PC, Tam J, Katzenback BA, Hitchen SJ, Barreda DR, Belosevic M; Tam; Katzenback; Hitchen; Barreda; Belosevic (April 2009). "Development of macrophages of cyprinid fish". <i>Dev. Comp. Immunol</i>. <b>33</b> (4): 411–29. <a href="/enwiki/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1016%2Fj.dci.2008.11.004">10.1016/j.dci.2008.11.004</a>. <a href="/enwiki/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="/enwiki//pubmed.ncbi.nlm.nih.gov/19063916">19063916</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Dev.+Comp.+Immunol.&rft.atitle=Development+of+macrophages+of+cyprinid+fish&rft.volume=33&rft.issue=4&rft.pages=411-29&rft.date=2009-04&rft_id=info%3Adoi%2F10.1016%2Fj.dci.2008.11.004&rft_id=info%3Apmid%2F19063916&rft.au=Hanington+PC%2C+Tam+J%2C+Katzenback+BA%2C+Hitchen+SJ%2C+Barreda+DR%2C+Belosevic+M&rft.au=Tam&rft.au=Katzenback&rft.au=Hitchen&rft.au=Barreda&rft.au=Belosevic&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span><span class="cs1-maint citation-comment"><code class="cs1-code">{{<a href="/enwiki/wiki/Template:Cite_journal" title="Template:Cite journal">cite journal</a>}}</code>: CS1 maint: multiple names: authors list (<a href="/enwiki/wiki/Category:CS1_maint:_multiple_names:_authors_list" title="Category:CS1 maint: multiple names: authors list">link</a>)</span></span>
</li>
<li id="cite_note-amoebaphage-122"><span class="mw-cite-backlink"><b><a href="#cite_ref-amoebaphage_122-0">^</a></b></span> <span class="error mw-ext-cite-error" lang="en" dir="ltr">Cite error: The named reference <code>amoebaphage</code> was invoked but never defined (see the <a href="/enwiki/wiki/Help:Cite_errors/Cite_error_references_no_text" title="Help:Cite errors/Cite error references no text">help page</a>).</span></li>
</ol></div>
<dl><dt>Bibliography</dt></dl>
<style data-mw-deduplicate="TemplateStyles:r1054258005">.mw-parser-output .refbegin{font-size:90%;margin-bottom:0.5em}.mw-parser-output .refbegin-hanging-indents>ul{margin-left:0}.mw-parser-output .refbegin-hanging-indents>ul>li{margin-left:0;padding-left:3.2em;text-indent:-3.2em}.mw-parser-output .refbegin-hanging-indents ul,.mw-parser-output .refbegin-hanging-indents ul li{list-style:none}@media(max-width:720px){.mw-parser-output .refbegin-hanging-indents>ul>li{padding-left:1.6em;text-indent:-1.6em}}.mw-parser-output .refbegin-columns{margin-top:0.3em}.mw-parser-output .refbegin-columns ul{margin-top:0}.mw-parser-output .refbegin-columns li{page-break-inside:avoid;break-inside:avoid-column}</style><div class="refbegin" style="">
<ul><li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFDelvesMartinBurtonRoit2006" class="citation book cs1">Delves, P. J.; Martin, S. J.; Burton, D. R.; Roit, I. M. (2006). <i>Roitt's Essential Immunology</i> (11th ed.). Malden, MA: Blackwell Publishing. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-1-4051-3603-7" title="Special:BookSources/978-1-4051-3603-7"><bdi>978-1-4051-3603-7</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Roitt%27s+Essential+Immunology&rft.place=Malden%2C+MA&rft.edition=11th&rft.pub=Blackwell+Publishing&rft.date=2006&rft.isbn=978-1-4051-3603-7&rft.aulast=Delves&rft.aufirst=P.+J.&rft.au=Martin%2C+S.+J.&rft.au=Burton%2C+D.+R.&rft.au=Roit%2C+I.+M.&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></li>
<li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFErnstStendahl2006" class="citation book cs1">Ernst, J. D.; Stendahl, O., eds. (2006). <i>Phagocytosis of Bacteria and Bacterial Pathogenicity</i>. New York: Cambridge University Press. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-0-521-84569-4" title="Special:BookSources/978-0-521-84569-4"><bdi>978-0-521-84569-4</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Phagocytosis+of+Bacteria+and+Bacterial+Pathogenicity&rft.place=New+York&rft.pub=Cambridge+University+Press&rft.date=2006&rft.isbn=978-0-521-84569-4&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span> <a rel="nofollow" class="external text" href="http://www.cambridge.org/9780521845694">Website</a></li>
<li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFHoffbrandPettitMoss2005" class="citation book cs1">Hoffbrand, A. V.; Pettit, J. E.; Moss, P. A. H. (2005). <i>Essential Haematology</i> (4th ed.). London: Blackwell Science. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-0-632-05153-3" title="Special:BookSources/978-0-632-05153-3"><bdi>978-0-632-05153-3</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Essential+Haematology&rft.place=London&rft.edition=4th&rft.pub=Blackwell+Science&rft.date=2005&rft.isbn=978-0-632-05153-3&rft.aulast=Hoffbrand&rft.aufirst=A.+V.&rft.au=Pettit%2C+J.+E.&rft.au=Moss%2C+P.+A.+H.&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></li>
<li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFPaolettiNotarioRicevuti1997" class="citation book cs1">Paoletti, R.; Notario, A.; Ricevuti, G., eds. (1997). <i>Phagocytes: Biology, Physiology, Pathology, and Pharmacotherapeutics</i>. New York: The New York Academy of Sciences. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-1-57331-102-1" title="Special:BookSources/978-1-57331-102-1"><bdi>978-1-57331-102-1</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Phagocytes%3A+Biology%2C+Physiology%2C+Pathology%2C+and+Pharmacotherapeutics&rft.place=New+York&rft.pub=The+New+York+Academy+of+Sciences&rft.date=1997&rft.isbn=978-1-57331-102-1&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></li>
<li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFRobinsonBabcock1998" class="citation book cs1">Robinson, J. P.; Babcock, G. F., eds. (1998). <span class="cs1-lock-registration" title="Free registration required"><a rel="nofollow" class="external text" href="https://archive.org/details/phagocytefunctio0000unse"><i>Phagocyte Function — A guide for research and clinical evaluation</i></a></span>. New York: Wiley–Liss. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-0-471-12364-4" title="Special:BookSources/978-0-471-12364-4"><bdi>978-0-471-12364-4</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Phagocyte+Function+%E2%80%94+A+guide+for+research+and+clinical+evaluation&rft.place=New+York&rft.pub=Wiley%E2%80%93Liss&rft.date=1998&rft.isbn=978-0-471-12364-4&rft_id=https%3A%2F%2Farchive.org%2Fdetails%2Fphagocytefunctio0000unse&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></li>
<li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1067248974"/><cite id="CITEREFSompayrac2019" class="citation book cs1">Sompayrac, L. (2019). <i>How the Immune System Works</i> (6th ed.). Malden, MA: Blackwell Publishing. <a href="/enwiki/wiki/ISBN_(identifier)" class="mw-redirect" title="ISBN (identifier)">ISBN</a> <a href="/enwiki/wiki/Special:BookSources/978-1-119-54212-4" title="Special:BookSources/978-1-119-54212-4"><bdi>978-1-119-54212-4</bdi></a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=How+the+Immune+System+Works&rft.place=Malden%2C+MA&rft.edition=6th&rft.pub=Blackwell+Publishing&rft.date=2019&rft.isbn=978-1-119-54212-4&rft.aulast=Sompayrac&rft.aufirst=L.&rfr_id=info%3Asid%2Fen.wikipedia.org%3APhagocyte" class="Z3988"></span></li></ul>
</div>
<h2><span class="mw-headline" id="External_links">External links</span><span class="mw-editsection"><span class="mw-editsection-bracket">[</span><a href="/enwiki/w/index.php?title=Phagocyte&action=edit&section=28" title="Edit section: External links">edit</a><span class="mw-editsection-bracket">]</span></span></h2>
<style data-mw-deduplicate="TemplateStyles:r1045330069">.mw-parser-output .sidebar{width:22em;float:right;clear:right;margin:0.5em 0 1em 1em;background:#f8f9fa;border:1px solid #aaa;padding:0.2em;text-align:center;line-height:1.4em;font-size:88%;border-collapse:collapse;display:table}body.skin-minerva .mw-parser-output .sidebar{display:table!important;float:right!important;margin:0.5em 0 1em 1em!important}.mw-parser-output .sidebar-subgroup{width:100%;margin:0;border-spacing:0}.mw-parser-output .sidebar-left{float:left;clear:left;margin:0.5em 1em 1em 0}.mw-parser-output .sidebar-none{float:none;clear:both;margin:0.5em 1em 1em 0}.mw-parser-output .sidebar-outer-title{padding:0 0.4em 0.2em;font-size:125%;line-height:1.2em;font-weight:bold}.mw-parser-output .sidebar-top-image{padding:0.4em}.mw-parser-output .sidebar-top-caption,.mw-parser-output .sidebar-pretitle-with-top-image,.mw-parser-output .sidebar-caption{padding:0.2em 0.4em 0;line-height:1.2em}.mw-parser-output .sidebar-pretitle{padding:0.4em 0.4em 0;line-height:1.2em}.mw-parser-output .sidebar-title,.mw-parser-output .sidebar-title-with-pretitle{padding:0.2em 0.8em;font-size:145%;line-height:1.2em}.mw-parser-output .sidebar-title-with-pretitle{padding:0.1em 0.4em}.mw-parser-output .sidebar-image{padding:0.2em 0.4em 0.4em}.mw-parser-output .sidebar-heading{padding:0.1em 0.4em}.mw-parser-output .sidebar-content{padding:0 0.5em 0.4em}.mw-parser-output .sidebar-content-with-subgroup{padding:0.1em 0.4em 0.2em}.mw-parser-output .sidebar-above,.mw-parser-output .sidebar-below{padding:0.3em 0.8em;font-weight:bold}.mw-parser-output .sidebar-collapse .sidebar-above,.mw-parser-output .sidebar-collapse .sidebar-below{border-top:1px solid #aaa;border-bottom:1px solid #aaa}.mw-parser-output .sidebar-navbar{text-align:right;font-size:115%;padding:0 0.4em 0.4em}.mw-parser-output .sidebar-list-title{padding:0 0.4em;text-align:left;font-weight:bold;line-height:1.6em;font-size:105%}.mw-parser-output .sidebar-list-title-c{padding:0 0.4em;text-align:center;margin:0 3.3em}@media(max-width:720px){body.mediawiki .mw-parser-output .sidebar{width:100%!important;clear:both;float:none!important;margin-left:0!important;margin-right:0!important}}</style><table class="sidebar nomobile nowraplinks" style="width:auto;text-align:left;"><tbody><tr><td class="sidebar-pretitle"><a href="/enwiki/wiki/Wikipedia:The_Wikipedia_Library" title="Wikipedia:The Wikipedia Library">Library resources</a> about <br /> <b>Phagocyte</b> <hr /></td></tr><tr><td class="sidebar-content plainlist">
<ul><li><a class="external text" href="https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes&library=OLBP">Online books</a></li>
<li><a class="external text" href="https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes">Resources in your library</a></li>
<li><a class="external text" href="https://ftl.toolforge.org/cgi-bin/ftl?st=&su=Phagocytes&library=0CHOOSE0">Resources in other libraries</a></li></ul></td>
</tr></tbody></table>
<style data-mw-deduplicate="TemplateStyles:r1097025294">.mw-parser-output .side-box{margin:4px 0;box-sizing:border-box;border:1px solid #aaa;font-size:88%;line-height:1.25em;background-color:#f9f9f9}.mw-parser-output .side-box-abovebelow,.mw-parser-output .side-box-text{padding:0.25em 0.9em}.mw-parser-output .side-box-image{padding:2px 0 2px 0.9em;text-align:center}.mw-parser-output .side-box-imageright{padding:2px 0.9em 2px 0;text-align:center}@media(min-width:500px){.mw-parser-output .side-box-flex{display:flex;align-items:center}.mw-parser-output .side-box-text{flex:1}}@media(min-width:720px){.mw-parser-output .side-box{width:238px}.mw-parser-output .side-box-right{clear:right;float:right;margin-left:1em}.mw-parser-output .side-box-left{margin-right:1em}}</style><div class="side-box side-box-right plainlinks sistersitebox">
<div class="side-box-flex">
<div class="side-box-image"><img alt="" src="/upwiki/wikipedia/en/thumb/4/4a/Commons-logo.svg/30px-Commons-logo.svg.png" decoding="async" width="30" height="40" class="noviewer" srcset="/upwiki/wikipedia/en/thumb/4/4a/Commons-logo.svg/45px-Commons-logo.svg.png 1.5x, /upwiki/wikipedia/en/thumb/4/4a/Commons-logo.svg/59px-Commons-logo.svg.png 2x" data-file-width="1024" data-file-height="1376" /></div>
<div class="side-box-text plainlist">Wikimedia Commons has media related to <span style="font-weight: bold; font-style: italic;"><a href="https://commons.wikimedia.org/wiki/Category:Phagocytes" class="extiw" title="commons:Category:Phagocytes">Phagocytes</a></span>.</div></div>
</div>
<ul><li><a rel="nofollow" class="external text" href="https://meshb.nlm.nih.gov/record/ui?name=Phagocytes">Phagocytes</a> at the US National Library of Medicine <a href="/enwiki/wiki/Medical_Subject_Headings" title="Medical Subject Headings">Medical Subject Headings</a> (MeSH)</li>
<li><a rel="nofollow" class="external text" href="https://www.youtube.com/watch?v=JnlULOjUhSQ">White blood cell engulfing bacteria</a></li></ul>
<div class="navbox-styles nomobile"><style data-mw-deduplicate="TemplateStyles:r1061467846">.mw-parser-output .navbox{box-sizing:border-box;border:1px solid #a2a9b1;width:100%;clear:both;font-size:88%;text-align:center;padding:1px;margin:1em auto 0}.mw-parser-output .navbox .navbox{margin-top:0}.mw-parser-output .navbox+.navbox,.mw-parser-output .navbox+.navbox-styles+.navbox{margin-top:-1px}.mw-parser-output .navbox-inner,.mw-parser-output .navbox-subgroup{width:100%}.mw-parser-output .navbox-group,.mw-parser-output .navbox-title,.mw-parser-output .navbox-abovebelow{padding:0.25em 1em;line-height:1.5em;text-align:center}.mw-parser-output .navbox-group{white-space:nowrap;text-align:right}.mw-parser-output .navbox,.mw-parser-output .navbox-subgroup{background-color:#fdfdfd}.mw-parser-output .navbox-list{line-height:1.5em;border-color:#fdfdfd}.mw-parser-output .navbox-list-with-group{text-align:left;border-left-width:2px;border-left-style:solid}.mw-parser-output tr+tr>.navbox-abovebelow,.mw-parser-output tr+tr>.navbox-group,.mw-parser-output tr+tr>.navbox-image,.mw-parser-output tr+tr>.navbox-list{border-top:2px solid #fdfdfd}.mw-parser-output .navbox-title{background-color:#ccf}.mw-parser-output .navbox-abovebelow,.mw-parser-output .navbox-group,.mw-parser-output .navbox-subgroup .navbox-title{background-color:#ddf}.mw-parser-output .navbox-subgroup .navbox-group,.mw-parser-output .navbox-subgroup .navbox-abovebelow{background-color:#e6e6ff}.mw-parser-output .navbox-even{background-color:#f7f7f7}.mw-parser-output .navbox-odd{background-color:transparent}.mw-parser-output .navbox .hlist td dl,.mw-parser-output .navbox .hlist td ol,.mw-parser-output .navbox .hlist td ul,.mw-parser-output .navbox td.hlist dl,.mw-parser-output .navbox td.hlist ol,.mw-parser-output .navbox td.hlist ul{padding:0.125em 0}.mw-parser-output .navbox .navbar{display:block;font-size:100%}.mw-parser-output .navbox-title .navbar{float:left;text-align:left;margin-right:0.5em}</style></div><div role="navigation" class="navbox" aria-labelledby="Myeloid_blood_cells_and_plasma" style="padding:3px"><table class="nowraplinks mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="2"><style data-mw-deduplicate="TemplateStyles:r1063604349">.mw-parser-output .navbar{display:inline;font-size:88%;font-weight:normal}.mw-parser-output .navbar-collapse{float:left;text-align:left}.mw-parser-output .navbar-boxtext{word-spacing:0}.mw-parser-output .navbar ul{display:inline-block;white-space:nowrap;line-height:inherit}.mw-parser-output .navbar-brackets::before{margin-right:-0.125em;content:"[ "}.mw-parser-output .navbar-brackets::after{margin-left:-0.125em;content:" ]"}.mw-parser-output .navbar li{word-spacing:-0.125em}.mw-parser-output .navbar a>span,.mw-parser-output .navbar a>abbr{text-decoration:inherit}.mw-parser-output .navbar-mini abbr{font-variant:small-caps;border-bottom:none;text-decoration:none;cursor:inherit}.mw-parser-output .navbar-ct-full{font-size:114%;margin:0 7em}.mw-parser-output .navbar-ct-mini{font-size:114%;margin:0 4em}</style><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/enwiki/wiki/Template:Myeloid_blood_cells_and_plasma" title="Template:Myeloid blood cells and plasma"><abbr title="View this template" style=";;background:none transparent;border:none;box-shadow:none;padding:0;">v</abbr></a></li><li class="nv-talk"><a href="/enwiki/wiki/Template_talk:Myeloid_blood_cells_and_plasma" title="Template talk:Myeloid blood cells and plasma"><abbr title="Discuss this template" style=";;background:none transparent;border:none;box-shadow:none;padding:0;">t</abbr></a></li><li class="nv-edit"><a class="external text" href="https://en.wikipedia.org/enwiki/w/index.php?title=Template:Myeloid_blood_cells_and_plasma&action=edit"><abbr title="Edit this template" style=";;background:none transparent;border:none;box-shadow:none;padding:0;">e</abbr></a></li></ul></div><div id="Myeloid_blood_cells_and_plasma" style="font-size:114%;margin:0 4em">Myeloid blood cells and <a href="/enwiki/wiki/Blood_plasma" title="Blood plasma">plasma</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Haematopoiesis" title="Haematopoiesis">Hematopoiesis</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th id="Myelopoiesis(CFU-GEMM)" scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Myelopoiesis" title="Myelopoiesis">Myelopoiesis</a><br />(<a href="/enwiki/wiki/CFU-GEMM" title="CFU-GEMM">CFU-GEMM</a>)</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/CFU-GM" title="CFU-GM">CFU-GM</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><td colspan="2" class="navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Granulopoiesis" title="Granulopoiesis">Granulopoiesis</a>
<ul><li><a href="/enwiki/wiki/Myeloblast" title="Myeloblast">Myeloblast</a></li>
<li><a href="/enwiki/wiki/Promyelocyte" title="Promyelocyte">Promyelocyte</a></li>
<li><a href="/enwiki/wiki/Myelocyte" title="Myelocyte">Myelocyte</a></li>
<li><a href="/enwiki/wiki/Metamyelocyte" title="Metamyelocyte">Metamyelocyte</a></li>
<li><a href="/enwiki/wiki/Band_cell" title="Band cell">Band cell</a></li></ul></li></ul>
</div></td></tr><tr><td colspan="2" class="navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Monocytopoiesis" title="Monocytopoiesis">Monocytopoiesis</a>
<ul><li><a href="/enwiki/wiki/Monoblast" title="Monoblast">Monoblast</a></li>
<li><a href="/enwiki/wiki/Promonocyte" title="Promonocyte">Promonocyte</a></li></ul></li></ul>
</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Megakaryocyte%E2%80%93erythroid_progenitor_cell" title="Megakaryocyte–erythroid progenitor cell">MEP</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><td colspan="2" class="navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Thrombopoiesis" title="Thrombopoiesis">Thrombopoiesis</a>
<ul><li><a href="/enwiki/wiki/Megakaryoblast" title="Megakaryoblast">Megakaryoblast</a></li>
<li><a href="/enwiki/wiki/Promegakaryocyte" title="Promegakaryocyte">Promegakaryocyte</a></li></ul></li></ul>
</div></td></tr><tr><td colspan="2" class="navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Erythropoiesis" title="Erythropoiesis">Erythropoiesis</a>
<ul><li><a href="/enwiki/wiki/Proerythroblast" title="Proerythroblast">Proerythroblast</a></li>
<li><a href="/enwiki/wiki/Normoblast" class="mw-redirect" title="Normoblast">Normoblast</a></li>
<li><a href="/enwiki/wiki/Reticulocyte" title="Reticulocyte">Reticulocyte</a></li></ul></li></ul>
</div></td></tr></tbody></table><div></div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">General</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Extramedullary_hematopoiesis" title="Extramedullary hematopoiesis">Extramedullary hematopoiesis</a></li></ul>
</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Myeloid_tissue" title="Myeloid tissue">Myeloid tissue</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Granulocyte" title="Granulocyte">Granulocytes</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Myeloblast" title="Myeloblast">Myeloblast</a></li>
<li><a href="/enwiki/wiki/Band_cell" title="Band cell">Band cell</a></li>
<li><a href="/enwiki/wiki/Neutrophil" title="Neutrophil">Neutrophil</a></li>
<li><a href="/enwiki/wiki/Basophil" title="Basophil">Basophil</a>
<ul><li><a href="/enwiki/wiki/CFU-Baso" title="CFU-Baso">CFU-Baso</a></li></ul></li>
<li><a href="/enwiki/wiki/Eosinophil" title="Eosinophil">Eosinophil</a>
<ul><li><a href="/enwiki/wiki/CFU-Eos" title="CFU-Eos">CFU-Eos</a></li></ul></li>
<li><a href="/enwiki/wiki/Mast_cell" title="Mast cell">Mast cell</a>
<ul><li><a href="/enwiki/wiki/CFU-Mast" title="CFU-Mast">CFU-Mast</a></li></ul></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Monocyte" title="Monocyte">Monocytes</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Macrophage" title="Macrophage">Macrophages</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Histiocyte" title="Histiocyte">Histiocytes</a></li>
<li><a href="/enwiki/wiki/Kupffer_cell" title="Kupffer cell">Kupffer cells</a></li>
<li><a href="/enwiki/wiki/Alveolar_macrophage" title="Alveolar macrophage">Alveolar macrophage</a></li>
<li><a href="/enwiki/wiki/Microglia" title="Microglia">Microglia</a></li>
<li><a href="/enwiki/wiki/Osteoclast" title="Osteoclast">Osteoclasts</a></li>
<li><a href="/enwiki/wiki/Epithelioid_cell" title="Epithelioid cell">Epithelioid cells</a></li>
<li><a href="/enwiki/wiki/Giant_cell" title="Giant cell">giant cells</a>
<ul><li><a href="/enwiki/wiki/Langhans_giant_cell" title="Langhans giant cell">Langhans giant cells</a></li>
<li><a href="/enwiki/wiki/Foreign-body_giant_cell" title="Foreign-body giant cell">Foreign-body giant cell</a></li>
<li><a href="/enwiki/wiki/Touton_giant_cell" title="Touton giant cell">Touton giant cells</a></li></ul></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Other</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li>Antigen-presenting cells
<ul><li><a href="/enwiki/wiki/Dendritic_cell" title="Dendritic cell">Dendritic cells</a></li>
<li><a href="/enwiki/wiki/Langerhans_cell" title="Langerhans cell">Langerhans cell</a></li>
<li><a href="/enwiki/wiki/CFU-DL" title="CFU-DL">CFU-DL</a></li></ul></li>
<li><a href="/enwiki/wiki/Monoblast" title="Monoblast">Monoblast</a>
<ul><li><a href="/enwiki/wiki/Mononuclear_phagocyte_system" title="Mononuclear phagocyte system">MPS</a></li></ul></li></ul>
</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Platelet" title="Platelet">Platelets</a></th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/CFU-Meg" title="CFU-Meg">CFU-Meg</a></li>
<li><a href="/enwiki/wiki/Megakaryoblast" title="Megakaryoblast">Megakaryoblast</a></li>
<li><a href="/enwiki/wiki/Promegakaryocyte" title="Promegakaryocyte">Promegakaryocyte</a></li>
<li><a href="/enwiki/wiki/Megakaryocyte" title="Megakaryocyte">Megakaryocyte</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Red_blood_cell" title="Red blood cell">Red blood cells</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Reticulocyte" title="Reticulocyte">Reticulocyte</a></li>
<li><a href="/enwiki/wiki/Nucleated_red_blood_cell" title="Nucleated red blood cell">Nucleated red blood cell</a></li>
<li><a href="/enwiki/wiki/CFU-E" title="CFU-E">CFU-E</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Immune response</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Leukocyte_extravasation" title="Leukocyte extravasation">Leukocyte extravasation</a></li>
<li><a href="/enwiki/wiki/Phagocytosis" title="Phagocytosis">Phagocytosis</a></li>
<li><a href="/enwiki/wiki/Intrinsic_immunity" title="Intrinsic immunity">Intrinsic immunity</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Other</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li>Precursor cells
<ul><li><a href="/enwiki/wiki/CFU-GM" title="CFU-GM">CFU-GM</a></li>
<li><a href="/enwiki/wiki/Megakaryocyte%E2%80%93erythroid_progenitor_cell" title="Megakaryocyte–erythroid progenitor cell">Megakaryocyte–erythroid progenitor cell</a></li>
<li><a href="/enwiki/wiki/CFU-GEMM" title="CFU-GEMM">CFU-GEMM</a></li></ul></li>
<li><a href="/enwiki/wiki/Myelomonocyte" title="Myelomonocyte">Myelomonocyte</a></li></ul>
</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Other</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a class="mw-selflink selflink">Phagocyte</a></li>
<li><a href="/enwiki/wiki/Blood_plasma" title="Blood plasma">Plasma</a></li>
<li><a href="/enwiki/wiki/Hematopoietic_system" class="mw-redirect" title="Hematopoietic system">Hematopoietic system</a>
<ul><li><a href="/enwiki/wiki/Hematopoietic_stem_cell" title="Hematopoietic stem cell">Hematopoietic stem cell</a></li></ul></li></ul>
</div></td></tr></tbody></table></div>
<div class="navbox-styles nomobile"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1061467846"/></div><div role="navigation" class="navbox" aria-labelledby="Lymphocytic_adaptive_immune_system_and_complement" style="padding:3px"><table class="nowraplinks mw-collapsible autocollapse navbox-inner" style="border-spacing:0;background:transparent;color:inherit"><tbody><tr><th scope="col" class="navbox-title" colspan="2"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1063604349"/><div class="navbar plainlinks hlist navbar-mini"><ul><li class="nv-view"><a href="/enwiki/wiki/Template:Lymphocytic_immune_system" title="Template:Lymphocytic immune system"><abbr title="View this template" style=";;background:none transparent;border:none;box-shadow:none;padding:0;">v</abbr></a></li><li class="nv-talk"><a href="/enwiki/wiki/Template_talk:Lymphocytic_immune_system" title="Template talk:Lymphocytic immune system"><abbr title="Discuss this template" style=";;background:none transparent;border:none;box-shadow:none;padding:0;">t</abbr></a></li><li class="nv-edit"><a class="external text" href="https://en.wikipedia.org/enwiki/w/index.php?title=Template:Lymphocytic_immune_system&action=edit"><abbr title="Edit this template" style=";;background:none transparent;border:none;box-shadow:none;padding:0;">e</abbr></a></li></ul></div><div id="Lymphocytic_adaptive_immune_system_and_complement" style="font-size:114%;margin:0 4em"><a href="/enwiki/wiki/Lymphocyte" title="Lymphocyte">Lymphocytic</a> <a href="/enwiki/wiki/Adaptive_immune_system" title="Adaptive immune system">adaptive immune system</a> and <a href="/enwiki/wiki/Complement_system" title="Complement system">complement</a></div></th></tr><tr><th scope="row" class="navbox-group" style="width:1%">Lymphoid</th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em"></div><table class="nowraplinks navbox-subgroup" style="border-spacing:0"><tbody><tr><th scope="row" class="navbox-group" style="width:1%">Antigens</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Antigen" title="Antigen">Antigen</a>
<ul><li><a href="/enwiki/wiki/Superantigen" title="Superantigen">Superantigen</a></li>
<li><a href="/enwiki/wiki/Allergen" title="Allergen">Allergen</a></li>
<li><a href="/enwiki/wiki/Antigenic_variation" title="Antigenic variation">Antigenic variation</a></li></ul></li>
<li><a href="/enwiki/wiki/Hapten" title="Hapten">Hapten</a></li></ul>
<ul><li><a href="/enwiki/wiki/Epitope" title="Epitope">Epitope</a>
<ul><li><a href="/enwiki/wiki/Linear_epitope" title="Linear epitope">Linear</a></li>
<li><a href="/enwiki/wiki/Conformational_epitope" title="Conformational epitope">Conformational</a></li></ul></li>
<li><a href="/enwiki/wiki/Mimotope" title="Mimotope">Mimotope</a></li></ul>
<ul><li><a href="/enwiki/wiki/Antigen_presentation" title="Antigen presentation">Antigen presentation</a>/<a href="/enwiki/wiki/Antigen-presenting_cell" title="Antigen-presenting cell">professional APCs</a>: <a href="/enwiki/wiki/Dendritic_cell" title="Dendritic cell">Dendritic cell</a></li>
<li><a href="/enwiki/wiki/Macrophage" title="Macrophage">Macrophage</a></li>
<li><a href="/enwiki/wiki/B_cell" title="B cell">B cell</a></li>
<li><a href="/enwiki/wiki/Immunogen" title="Immunogen">Immunogen</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Antibodies</th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Antibody" title="Antibody">Antibody</a>
<ul><li><a href="/enwiki/wiki/Monoclonal_antibody" title="Monoclonal antibody">Monoclonal antibodies</a></li>
<li><a href="/enwiki/wiki/Polyclonal_antibodies" title="Polyclonal antibodies">Polyclonal antibodies</a></li>
<li><a href="/enwiki/wiki/Autoantibody" title="Autoantibody">Autoantibody</a></li>
<li><a href="/enwiki/wiki/Microantibody" title="Microantibody">Microantibody</a></li></ul></li>
<li><a href="/enwiki/wiki/Polyclonal_B_cell_response" title="Polyclonal B cell response">Polyclonal B cell response</a></li>
<li><a href="/enwiki/wiki/Allotype_(immunology)" title="Allotype (immunology)">Allotype</a></li>
<li><a href="/enwiki/wiki/Isotype_(immunology)" title="Isotype (immunology)">Isotype</a></li>
<li><a href="/enwiki/wiki/Idiotype" title="Idiotype">Idiotype</a></li></ul>
<ul><li><a href="/enwiki/wiki/Immune_complex" title="Immune complex">Immune complex</a></li>
<li><a href="/enwiki/wiki/Paratope" title="Paratope">Paratope</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Immunity vs.<br /> tolerance</th><td class="navbox-list-with-group navbox-list navbox-odd" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li>Action: <a href="/enwiki/wiki/Immunity_(medical)" title="Immunity (medical)">Immunity</a></li>
<li><a href="/enwiki/wiki/Autoimmunity" title="Autoimmunity">Autoimmunity</a></li>
<li><a href="/enwiki/wiki/Alloimmunity" title="Alloimmunity">Alloimmunity</a></li>
<li><a href="/enwiki/wiki/Allergy" title="Allergy">Allergy</a></li>
<li><a href="/enwiki/wiki/Hypersensitivity" title="Hypersensitivity">Hypersensitivity</a></li>
<li><a href="/enwiki/wiki/Inflammation" title="Inflammation">Inflammation</a></li>
<li><a href="/enwiki/wiki/Cross-reactivity" title="Cross-reactivity">Cross-reactivity</a></li>
<li><a href="/enwiki/wiki/Co-stimulation" title="Co-stimulation">Co-stimulation</a></li></ul>
<ul><li>Inaction: <a href="/enwiki/wiki/Immune_tolerance" title="Immune tolerance">Tolerance</a>
<ul><li><a href="/enwiki/wiki/Central_tolerance" title="Central tolerance">Central</a></li>
<li><a href="/enwiki/wiki/Peripheral_tolerance" title="Peripheral tolerance">Peripheral</a></li>
<li><a href="/enwiki/wiki/Clonal_anergy" title="Clonal anergy">Clonal anergy</a></li>
<li><a href="/enwiki/wiki/Clonal_deletion" title="Clonal deletion">Clonal deletion</a></li>
<li><a href="/enwiki/wiki/Immune_tolerance_in_pregnancy" title="Immune tolerance in pregnancy">Tolerance in pregnancy</a></li></ul></li>
<li><a href="/enwiki/wiki/Immunodeficiency" title="Immunodeficiency">Immunodeficiency</a></li>
<li><a href="/enwiki/wiki/Immune_privilege" title="Immune privilege">Immune privilege</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Immunogenetics" title="Immunogenetics">Immunogenetics</a></th><td class="navbox-list-with-group navbox-list navbox-even" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Affinity_maturation" title="Affinity maturation">Affinity maturation</a>
<ul><li><a href="/enwiki/wiki/Somatic_hypermutation" title="Somatic hypermutation">Somatic hypermutation</a></li>
<li><a href="/enwiki/wiki/Clonal_selection" title="Clonal selection">Clonal selection</a></li></ul></li>
<li><a href="/enwiki/wiki/V(D)J_recombination" title="V(D)J recombination">V(D)J recombination</a></li>
<li><a href="/enwiki/wiki/Junctional_diversity" title="Junctional diversity">Junctional diversity</a></li>
<li><a href="/enwiki/wiki/Immunoglobulin_class_switching" title="Immunoglobulin class switching">Immunoglobulin class switching</a></li>
<li><a href="/enwiki/wiki/Major_histocompatibility_complex" title="Major histocompatibility complex">MHC</a>/<a href="/enwiki/wiki/Human_leukocyte_antigen" title="Human leukocyte antigen">HLA</a></li></ul>
</div></td></tr></tbody></table><div></div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%"><a href="/enwiki/wiki/Lymphocyte" title="Lymphocyte">Lymphocytes</a></th><td class="navbox-list-with-group navbox-list navbox-odd hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Cell-mediated_immunity" title="Cell-mediated immunity">Cellular</a>
<ul><li><a href="/enwiki/wiki/T_cell" title="T cell">T cell</a></li></ul></li>
<li><a href="/enwiki/wiki/Humoral_immunity" title="Humoral immunity">Humoral</a>
<ul><li><a href="/enwiki/wiki/B_cell" title="B cell">B cell</a></li></ul></li>
<li><a href="/enwiki/wiki/Natural_killer_cell" title="Natural killer cell">NK cell</a></li></ul>
</div></td></tr><tr><th scope="row" class="navbox-group" style="width:1%">Substances</th><td class="navbox-list-with-group navbox-list navbox-even hlist" style="width:100%;padding:0"><div style="padding:0 0.25em">
<ul><li><a href="/enwiki/wiki/Cytokine" title="Cytokine">Cytokines</a></li>
<li><a href="/enwiki/wiki/Opsonin" title="Opsonin">Opsonin</a></li>
<li><a href="/enwiki/wiki/Cytolysin" title="Cytolysin">Cytolysin</a></li></ul>
</div></td></tr></tbody></table></div>
<p class="mw-empty-elt">
</p></div>' |
Whether or not the change was made through a Tor exit node (tor_exit_node) | false |
Unix timestamp of change (timestamp) | '1664899985' |
