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Stomach microbiota, Helicobacter pylori, and group 2 innate lymphoid cells.

  • 작성자

    관리자
  • 작성일자

    2020-11-23
  • 조회수

    42
Hiroshi Ohno (hiroshi.ohno@riken.jp)
2013-pesent Team Leader, Laboratory for Intestinal Ecosystem, RIKEN Center for integrative Medical Sciences, Japan
2004-2013 Team Leader, Laboratory for Epithelial Immunobiology, RIKEN Research Center for Allergy and Immunology, Japan
1999-2004 Professor, Division of Molecular Membrane Biology, Cancer Research Institute, Kanazawa University, Japan
1997-1999 Associate Professor, Department of Molecular Genetics, Graduate School of Medicine, Chiba university, Japan
1994-1997 Visiting Scientist, CBMB, National Institute of Child Health and Human Development, National Institutes of Health, USA
1991-1997 Research Associate, Department of Molecular Genetics, School of Medicine, Chiba University, Japan
1987-1991 Ph.D. (Immunology Major), Department of Anesthesiology, Graduate School of Medicine, Chiba University, Japan
1983-1987 Clinical Fellow, Department of Anesthesiology, Chiba University Hospital, Japan
1977-1983 M.D., School of Medicine, Chiba University, Japan

Stomach microbiota, Helicobacter pylori, and group 2 innate lymphoid cells

The stomach has been thought to host few commensal bacteria because of the existence of barriers, such as gastric acid. However, recent culture-independent, sequencing-based microbial analysis has shown that the stomach also harbors a wide diversity of microbiota. Although the stomach immune system, especially innate lymphoid cells (ILCs), has not been well elucidated, recent studies have shown that group 2 ILCs (ILC2s) are the dominant subtype in the stomach of both humans and mice. Stomach ILC2s are unique in that their existence is dependent on stomach microbiota, in sharp contrast to the lack of an impact of commensal microbiota on ILC2s in other tissues. The microbiota dependency of stomach ILC2s is partly explained by their responsiveness to interleukin (IL)-7. Stomach ILC2s express significantly higher IL-7 receptor protein levels on their surface and proliferate more in response to IL-7 stimulation in vitro than small intestinal ILC2s. Consistently, the stomach expresses much higher IL-7 protein levels than the small intestine. IL-5 secreted from stomach ILC2s promotes immunoglobulin (Ig) A production by plasma B cells. In a murine model, stomach ILC2s are important in containing Helicobacter pylori infection, especially in the early phase of infection, by promoting IgA production.

Exp Mol Med. 2020 Sep;52(9):1377-1382. doi: 10.1038/s12276-020-00485-8.
https://pubmed.ncbi.nlm.nih.gov/32908209/