The Journal of Experimental Medicine
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Published online September 1, 2008
doi:10.1084/jem.20080720
The Journal of Experimental Medicine
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Zaph et al.
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BRIEF DEFINITIVE REPORT

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

Colby Zaph1, Yurong Du1, Steven A. Saenz1, Meera G. Nair1, Jacqueline G. Perrigoue1, Betsy C. Taylor1, Amy E. Troy1, Dmytro E. Kobuley2, Robert A. Kastelein3, Daniel J. Cua3, Yimin Yu2, and David Artis1

1 Department of Pathobiology and 2 Department of Biology, University of Pennsylvania, Philadelphia, PA 19104
3 Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304

CORRESPONDENCE David Artis: dartis{at}vet.upenn.edu OR Colby Zaph: colby{at}brc.ubc.ca

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.

C. Zaph's present address is The Biomedical Research Centre, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada.

© 2008 Zaph et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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