Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 205, Issue 10, Pages 2191-2198Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20080720
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Funding
- 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
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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.
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