Commensal-dependent expression of IL-25 regulates the IL-23-IL-17 axis in the intestine. Academic Article uri icon

Overview

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.

publication date

  • September 1, 2008

Research

keywords

  • Interleukin-17
  • Interleukin-23
  • Interleukins
  • Intestines

Identity

PubMed Central ID

  • PMC2556798

Scopus Document Identifier

  • 53349120339

Digital Object Identifier (DOI)

  • 10.1084/jem.20080720

PubMed ID

  • 18762568

Additional Document Info

volume

  • 205

issue

  • 10