M细胞(Membranous / microfold cell)扁平细胞，是散布于肠道黏膜上皮细胞间的一种特化的抗原运转细胞。它不表达MHCⅡ类分子，胞质内溶毛体很少，在肠黏膜表面有短小不规则毛刷样微绒毛。它具有高度的非特异性脂酶活性。病原菌等外来抗原性物质可通过对M细胞表面的毛刷状微绒毛的吸附，或经M细胞表面蛋白酶作用后被摄取。
粘膜免疫系统在保护粘膜表面不受病原体侵害、在促进与共生微生物群落共生中都起主要作用。要激发粘膜免疫反应，粘膜表面上的抗原必须首先穿过不可透过的上皮障碍，进入“派伊尔小结”这样的淋巴结构。这一功能（被称为“转胞吞作用”）被认为主要由M细胞调控，它们是“派伊尔小结”中专门的上皮细胞。对由M-细胞调控的抗原“转胞吞作用”的机制所做的一项研究表明，在小肠M细胞顶面表达的糖蛋白-2是表达FimH抗原的细菌的转胞吞受体。由于M-细胞被认为是各种口服免疫药物的一个很有希望的目标，所以这项工作表明，依赖于糖蛋白-2的“转胞吞作用”是一个可能的免疫目标。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 462, 226-230 (12 November 2009) | doi:10.1038/nature08529
Uptake through glycoprotein 2 of FimH+ bacteria by M cells initiates mucosal immune response
Koji Hase1,10, Kazuya Kawano1,10, Tomonori Nochi2, Gemilson Soares Pontes2, Shinji Fukuda1,3, Masashi Ebisawa1,3, Kazunori Kadokura1,3, Toru Tobe4, Yumiko Fujimura1, Sayaka Kawano1, Atsuko Yabashi5, Satoshi Waguri5, Gaku Nakato1,3, Shunsuke Kimura1, Takaya Murakami1, Mitsutoshi Iimura6, Kimiyo Hamura6, Shin-Ichi Fukuoka7, Anson W. Lowe8, Kikuji Itoh9, Hiroshi Kiyono2 & Hiroshi Ohno1,3
1 Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, Kanagawa 230-0045, Japan
2 Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan
3 Supramolecular Biology, International Graduate School of Bionanoscience, Yokohama City University, Kanagawa 230-0045, Japan
4 Graduate School of Medicine, Osaka University, 565-0871 Suita, Osaka, Japan
5 Department of Anatomy and Histology, Fukushima Medical University, School of Medicine, Fukushima 960-1295, Japan
6 Institute of Gastroenterology, Tokyo Women's Medical University, Tokyo 162-8666, Japan
7 Department of Chemistry and Biological Science, College of Science and Engineering, Aoyama Gakuin University, Kanagawa, 229-8558, Japan
8 Department of Medicine and the Digestive Disease Center, Stanford University, Stanford, California 94305, USA
9 Veterinary Public Health, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan
10 These authors contributed equally to this work.
Correspondence to: Hiroshi Ohno1,3 Correspondence and requests for materials should be addressed to H.O.
The mucosal immune system forms the largest part of the entire immune system, containing about three-quarters of all lymphocytes and producing grams of secretory IgA daily to protect the mucosal surface from pathogens1, 2, 3. To evoke the mucosal immune response, antigens on the mucosal surface must be transported across the epithelial barrier into organized lymphoid structures such as Peyer's patches4. This function, called antigen transcytosis, is mediated by specialized epithelial M cells5, 6. The molecular mechanisms promoting this antigen uptake, however, are largely unknown. Here we report that glycoprotein 2 (GP2), specifically expressed on the apical plasma membrane of M cells among enterocytes, serves as a transcytotic receptor for mucosal antigens. Recombinant GP2 protein selectively bound a subset of commensal and pathogenic enterobacteria, including Escherichia coli and Salmonella enterica serovar Typhimurium (S. Typhimurium), by recognizing FimH, a component of type I pili on the bacterial outer membrane. Consistently, these bacteria were colocalized with endogenous GP2 on the apical plasma membrane as well as in cytoplasmic vesicles in M cells. Moreover, deficiency of bacterial FimH or host GP2 led to defects in transcytosis of type-I-piliated bacteria through M cells, resulting in an attenuation of antigen-specific immune responses in Peyer's patches. GP2 is therefore a previously unrecognized transcytotic receptor on M cells for type-I-piliated bacteria and is a prerequisite for the mucosal immune response to these bacteria. Given that M cells are considered a promising target for oral vaccination against various infectious diseases7, 8, the GP2-dependent transcytotic pathway could provide a new target for the development of M-cell-targeted mucosal vaccines.
