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

Experimental & Molecular Medicine 2020년 52권 9호 p.8 ~ 8
Ohno Hiroshi, Satoh-Takayama Naoko,
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 ( Ohno Hiroshi ) - RIKEN Center for Integrative Medical Sciences Laboratory for Intestinal Ecosystem
 ( Satoh-Takayama Naoko ) - RIKEN Center for Integrative Medical Sciences Laboratory for Intestinal Ecosystem

Abstract


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.

키워드

Innate lymphoid cells; Mucosal immunology

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