Maintenance of gut homeostasis by the mucosal immune system

被引：50

作者：

Okumura, Ryu ^{[1
]}

Takeda, Kiyoshi ^{[1
]}

机构：

[1] Osaka Univ, Lab Immune Regulat, Dept Microbiol & Immunol, Grad Sch Med,WPI Immunol Frontier Res Ctr, Suita, Osaka 5650871, Japan

来源：

PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES | 2016年 / 92卷 / 09期

关键词：

innate immunity; intestinal microbiota; mucosal barrier; inflammatory bowel disease; INFLAMMATORY-BOWEL-DISEASE; REGULATORY T-CELLS; CD103(+)CD11B(+) DENDRITIC CELLS; INTESTINAL EPITHELIAL-CELLS; LECTIN REGIII-GAMMA; LAMINA PROPRIA; CHRONIC ENTEROCOLITIS; COMMENSAL BACTERIA; MYELOID CELLS; TUFT CELLS;

D O I：

10.2183/pjab.92.423

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Inflammatory bowel diseases (IBD) are represented by ulcerative colitis (UC) and Crohn's disease (CD), both of which involve chronic intestinal inflammation. Recent evidence has indicated that gut immunological homeostasis is maintained by the interaction between host immunity and intestinal microbiota. A variety of innate immune cells promote or suppress T cell differentiation and activation in response to intestinal bacteria or their metabolites. Some commensal bacteria species or bacterial metabolites enhance or repress host immunity by inducing T helper (Th) 17 cells or regulatory T cells. Intestinal epithelial cells between host immune cells and intestinal microbiota contribute to the separation of these populations and modulate host immune responses to intestinal microbiota. Therefore, the imbalance between host immunity and intestinal microbiota caused by host genetic predisposition or abnormal environmental factors promote susceptibility to intestinal inflammation.

引用

页码：423 / 435

页数：13

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