Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms14509
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Funding
- Ministry of Education, Science, Sports and Technology of Japan [23659199, 25860353, 16K08836, 23229004]
- Global Center of Excellence Program of the Center of Education and Research for Advanced Genome-based Medicine
- Core Research for Evolutional Science and Technology Program of the Japan Science and Technology Agency
- Grants-in-Aid for Scientific Research [23229004, 25860353, 23659199, 16K08836] Funding Source: KAKEN
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M cells in follicle-associated epithelium (FAE) are specialized antigen-sampling cells that take up intestinal luminal antigens. Transcription factor Spi-B regulates M-cell maturation, but the molecules that promote transcytosis within M cells are not fully identified. Here we show that mouse allograft inflammatory factor 1 (Aif1) is expressed by M cells and contributes to M-cell transcytosis. FAE in Aif1(-/-) mice has suppressed uptake of particles and commensal bacteria, compared with wild-type mice. Translocation of Yersinia enterocolitica, but not of Salmonella enterica serovar Typhimurium, leading to the generation of antigen-specific IgA antibodies, is also diminished in Aif1-deficient mice. Although b1 integrin, which acts as a receptor for Y. enterocolitica via invasin protein, is expressed on the apical surface membranes of M cells, its active form is rarely found in Aif1(-/-) mice. These findings show that Aif1 is important for bacterial and particle transcytosis in M cells.
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