Commensal-dependent expression of IL-25 regulates the IL-23-IL-17 axis in the intestine
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 a...
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Published in | The Journal of experimental medicine Vol. 205; no. 10; pp. 2191 - 2198 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
The Rockefeller University Press
29.09.2008
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Subjects | |
Online Access | Get full text |
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Summary: | 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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 CORRESPONDENCE David Artis: dartis@vet.upenn.edu OR Colby Zaph: colby@brc.ubc.ca C. Zaph's present address is The Biomedical Research Centre, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. |
ISSN: | 0022-1007 1540-9538 |
DOI: | 10.1084/jem.20080720 |