期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 205, 期 10, 页码 2191-2198出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20080720
关键词
-
资金
- National Institutes of Health [AI61570, AI74878, AI37108, F31-GM82187, T32-AI007532-08, F32-AI72943, T32-CA09140-30]
- Burroughs Wellcome Fund
- Crohn's and Colitis Foundation of America
- University of Pennsylvania
- Schering-Plough Corporation
- Irvington Institute Fellowship Program of the Cancer Research Institute
Alterations in the composition of intestinal commensal bacteria are associated with enhanced susceptibility to multiple inflammatory diseases, including those conditions associated with interleukin (IL)-17-producing CD4(+) T helper (Th17) cells. However, the relationship between commensal bacteria and the expression of proinflammatory cytokines remains unclear. Using germ-free mice, we show that the frequency of Th17 cells in the large intestine is significantly elevated in the absence of commensal bacteria. Commensal-dependent expression of the IL-17 family member IL-25 (IL-17E) by intestinal epithelial cells limits the expansion of Th17 cells in the intestine by inhibiting expression of macrophage-derived IL-23. We propose that acquisition of, or alterations in, commensal bacteria influences intestinal immune homeostasis via direct regulation of the IL-25 -IL-23 -IL-17 axis.
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。
推荐
暂无数据