4.5 Review

Intestinal immunity: to be, or not to be, induced? That is the question

期刊

INTERNATIONAL IMMUNOLOGY
卷 33, 期 12, 页码 755-759

出版社

OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxab051

关键词

commensal microbiota; fasting; IgA; intestinal immune system; M cell

资金

  1. Japan Society for the Promotion of Science [20H05876, 20H00509]
  2. AMED-Crest [21gm1310009h0002]
  3. Grants-in-Aid for Scientific Research [20H05876, 20H00509] Funding Source: KAKEN

向作者/读者索取更多资源

The intestinal immune system collaborates with various immune cell subsets to maintain intestinal homeostasis with the help of bacterial components, metabolites, and nutritional signals. Specialized M cells in GALT facilitate immune surveillance on the mucosal surface, but there is a self-regulatory mechanism to control their hyperplasia to prevent excessive immune response.
The intestinal immune system maintains intestinal homeostasis in collaboration with diverse immune cell subsets residing at the epithelial layer, lamina propria and gut-associated lymphoid tissue (GALT). Bacterial components and their metabolites are essential for the establishment of the gut immune system. In addition, nutritional signals contribute to maintaining the mucosal immune response. Specialized epithelial microfold (M) cells in GALT facilitate immune surveillance on the mucosal surface by actively taking up external antigens to transport them into the lymphoid follicles. Because hyperplasia of M cells causes an excessive immune response in GALT, there is a self-regulatory mechanism to control the development of M cells appropriately. In this review, we will discuss the molecular mechanisms of mucosal immune regulation and their biological importance.y

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据