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Microfold cell

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Microfold cell
Details
Identifiers
Latinepitheliocytus microplicatus
MeSHD000092303
THH3.04.03.0.00010
FMA62929
Anatomical terminology

Microfold cells (or M cells) are found in the follicle-associated epithelium (FAE) of the Peyer's patch as well as in gut-associated lymphoid tissue (GALT). These cells are known to initiate mucosal immunity responses on the apical membrane of the M cells and allow for transport of microbes and particles from the gut lumen into immune cells across the epithelial barrier.[1]

M cells express the protease cathepsin E, similar to other antigen presenting cells. Unlike their neighbouring cells, M cells have the unique ability to take up antigen from the lumen of the small intestine via endocytosis or phagocytosis, and then deliver it via transcytosis to antigen presenting cells, such as dendritic cells and lymphocytes (namely T cells). This process takes place in a unique pocket-like structure on their basolateral side [5]. Recognition of antigens is done via expression of cell surface receptors such as glycoprotein-2 (GP2) that detect and specifically bind to bacteria possessing Type I pili. Cellular prion protein (PrP) has also been identified as an antigen-uptake receptor on the surface of these cells.[2]

M cells lack microvilli and they are characterized by strong cell junction to function as a barrier and thus defense line in the immune system. Despite these characteristics, some antigens are able to infiltrate the M cell barrier and infect the nearby epithelial cells or enter the gut.[3]

Structure and function

M cells differ from normal enterocytes in that they lack microvilli on their apical surface, but instead possess broader microfolds that give the cell its name. These cells are far less abundant than enterocytes. M cells do not secrete mucus or digestive enzymes, and have a thinner glycocalyx, which allows them to have easy access to the intestinal lumen for endocytosis of antigens. M cells main function is the selective endocytosis of antigens, and transporting them to intraepithelial macrophages and lymphocytes, which then migrate to lymph nodes where an immune response can be initiated.

Morphology

M cells are distinguished from other intestinal epithelial cells by their morphological differences. They are characterized by short microvilli or lack of these protrusions on the cellsurface. When they present microvilli, they are short, irregular, and present on the apical surface or pocket-like invagination on the basolateral surface of these cells. When they lack microvilli, they are characterized by microfolds, and hence receive their commonly known name. These cells can also be identified by cytoskeletal and extracellular matrix components expressed at the edge of cells or on their cell surfaces, such as actin, villin, cytokeratin, and vimentin.[4]

Pathology

M cells are exploited by several pathogens, including Shigella flexneri, Salmonella typhimurium, and Yersinia pseudotuberculosis, as well as infectious prions in Bovine spongiform encephalitis (Mad-cow disease), as a way to penetrate the intestinal epithelium. Exploitation as a virulence factor depends upon the pathogen's ability to bind to M cells and thus guarantee penetration in that manner, as M cells sample intestinal contents. EPEC (see Pathogenic Escherichia coli) containing plasmids with genes for EAF (Escherichia coli Adherence Factor) will adhere to M cells.

They are also exploited by viruses such as Polio and Reovirus for dissemination.[5]

CXCR4 tropic but not CCR5 tropic HIV has been noted to be able to bind to M cells and get transported across the epithelium by them.[6]

Development

Factors promoting the differentiation of M cells have yet to be elucidated, but they are thought to develop in response to signals from immune cells found in the developing Peyer's patch.[7] B cells have been implicated in the developmental of M cells, since they are also localized in high numbers in the follicular-associated epithelium. FAE lacking B cell populations result in a decrease in the number of M cell lining the Peyer's patch [6]. Similarly, a human lymphoma cell line, called Raji cells, are also known to cause transition of adenocarcinoma cells to M cells. Though many studies have shown various cell types directing the differentiation of M cells, the field is at a point of characterizing the molecular pathways that guide M cell differentiation. More recently, through loss-of-function and rescue-phenotype studies, RANKL has been shown to be a receptor activator of NF-κB ligand and play a role in differentiation of M cells.[8] Interestingly, microbes found among existing intestinal epithelium are also known to direct M cell development. For example, the type III secretion system effector protein SopB activates the transition of M cells from enterocytes.[9] M cells undergo the differentiation process for up to four days before reaching full maturation. Recent studies have suggested they arise distinctly from the lymphoid and myeloid lineages.[10]

Pathogens can take advantage of cell differentiation pathways in order to invade the host cells. This is done by inducing differentiation of enterocytes into M cell type in gut epithelium[11]. In one case, the SopB effector protein mentioned above, is secreted by S. Typhimurium to trigger fast differentiation of enterocytes located in the FAE by initiation epithelial to mesenchymal transition of these cells.When SopB activates differentiation of enterocytes, it acts via the activation of the Wnt/b-catenin signaling pathway and triggers the RANKL and its receptor, implicated in regulating cell apoptosis [11].

References

  1. ^ Mabbott, N.A., Donaldson, D.S., Ohno, H., Williams, I.R., and Mahajan, A. (2013). Microfold (M) cells: important immunosurveillance posts in the intestinal epithelium. Mucosal Immunol 6, 666-677.
  2. ^ Miller, H., Zhang, J., Kuolee, R., Patel, G.B., and Chen, W. (2007). Intestinal M cells: the fallible sentinels? 13, 1477-1486.
  3. ^ Kanaya, T., and Ohno, H. (2014). The Mechanisms of M-cell Differentiation. 33, 91-97.
  4. ^ Kanaya, T., and Ohno, H. (2014). The Mechanisms of M-cell Differentiation. 33, 91-97.
  5. ^ Laurent Ouzilou1, Elise Caliot2, Isabelle Pelletier1, Marie-Christine Prévost3, Eric Pringault2 and Florence Colbère-Garapin1. Journal of General Virology (2002), 83, 2177-2182.
  6. ^ Grigorios Fotopoulos*, Alexandre Hararidagger , Pierre MichettiDagger , Didier Trono§, Giuseppe Pantaleodagger, and Jean-Pierre Kraehenbuhl. July 1, 2002, 10.1073/pnas.142586899
  7. ^ Kraehenbuhl J, Neutra M (2000). "Epithelial M cells: differentiation and function". Annu Rev Cell Dev Biol. 16: 301–32. doi:10.1146/annurev.cellbio.16.1.301. PMID 11031239. Link
  8. ^ Knoop KA, Kumar N, Butler BR, Sakthivel SK, Taylor RT, Nochi T, Akiba H, Yagita H, Kiyono H, Williams IR. 2009. RANKL is necessary and sufficient to initiate development of antigen-sampling M cells in the intestinal epithelium. J Immunol 183: 5738–5747.
  9. ^ Tahoun A, Mahajan S, Paxton E, Malterer G, Donaldson DS, Wang D, Tan A, Gillespie TL, O’Shea M, Roe AJ, Shaw DJ, Gally DL, Lengeling A, Mabbott NA, Haas J, Mahajan A. 2012. Salmonella transforms follicle- associated epithelial cells into M cells to promote intestinal invasion. Cell Host Microbe 12: 645–656.
  10. ^ "M Cell Differentiation: Distinct Lineage or Phenotypic Transition? Salmonella Provides Answers". www.sciencedirect.com. Retrieved 2016-01-16.
  11. ^ Mabbott, N.A., Donaldson, D.S., Ohno, H., Williams, I.R., and Mahajan, A. (2013). Microfold (M) cells: important immunosurveillance posts in the intestinal epithelium. Mucosal Immunol 6, 666-677.

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