Allograft inflammatory factor 1 is a regulator of transcytosis in M cells

  • Nat Commun. 2017 Feb 22;8:14509. doi: 10.1038/ncomms14509.
Sari Kishikawa  1  2 ,  Shintaro Sato  1  3  4  5  6 ,  Satoshi Kaneto  1 ,  Shigeo Uchino  7 ,  Shinichi Kohsaka  7 ,  Seiji Nakamura  2 ,  Hiroshi Kiyono  1  3  4  8
Affiliations
  • 1. Division of Mucosal Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
  • 2. Section of Oral and Maxillofacial Oncology, Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan.
  • 3. International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.
  • 4. Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo 102-0076, Japan.
  • 5. Mucosal Vaccine Project, BIKEN Innovative Vaccine Research Alliance Laboratories, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
  • 6. Mucosal Vaccine Project, BIKEN Center for Innovative Vaccine Research and Development, The Research Foundation for Microbial Diseases of Osaka University, Osaka 565-0871, Japan.
  • 7. Department of Neurochemistry, National Institute of Neuroscience, Tokyo 187-8502, Japan.
  • 8. Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
PMID: 28224999 DOI: 10.1038/ncomms14509
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.

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