Allograft inflammatory factor 1 is a regulator of transcytosis in M cells
Sari Kishikawa,
Shintaro Sato (),
Satoshi Kaneto,
Shigeo Uchino,
Shinichi Kohsaka,
Seiji Nakamura and
Hiroshi Kiyono ()
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Sari Kishikawa: The Institute of Medical Science, The University of Tokyo
Shintaro Sato: The Institute of Medical Science, The University of Tokyo
Satoshi Kaneto: The Institute of Medical Science, The University of Tokyo
Shigeo Uchino: National Institute of Neuroscience
Shinichi Kohsaka: National Institute of Neuroscience
Seiji Nakamura: Section of Oral and Maxillofacial Oncology, Faculty of Dental Science, Kyushu University
Hiroshi Kiyono: The Institute of Medical Science, The University of Tokyo
Nature Communications, 2017, vol. 8, issue 1, 1-10
Abstract:
Abstract 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 β1 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.
Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14509
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DOI: 10.1038/ncomms14509
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