Commensal-dependent expression of IL-25 regulates the IL-23–IL-17 axis in the intestine
The Journal of experimental medicine, 2008•rupress.org
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 …
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 …
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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