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Commensal-dependent expression of IL-25 regulates the IL-23-IL-17 axis in the intestine.

  • Author(s): Zaph, Colby;
  • Du, Yurong;
  • Saenz, Steven A;
  • Nair, Meera G;
  • Perrigoue, Jacqueline G;
  • Taylor, Betsy C;
  • Troy, Amy E;
  • Kobuley, Dmytro E;
  • Kastelein, Robert A;
  • Cua, Daniel J;
  • Yu, Yimin;
  • Artis, David
  • et al.
Abstract

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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