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Opposing consequences of IL-23 signaling mediated by innate and adaptive cells in chemically induced colitis in mice.

Abstract：

:The interleukin-23 (IL-23) pathway has emerged as a promising therapeutic target for inflammatory bowel disease. Although the pathogenic role of IL-23 receptor (IL-23R) on T lymphocytes is well established, its function on innate immune cells has not been thoroughly examined. Here we investigate the consequence of IL-23R deletion in dextran sulfate sodium (DSS)-induced colitis. In IL23R(-/-) and IL23p19(-/-) mice, we observed decreased weight loss and reduced leukocyte infiltrate following DSS exposure. Surprisingly, when the IL-23R(-/-) allele was crossed into Rag2(-/-) mice, we observed exacerbated disease, increased epithelial damage, reduced pSTAT3 in the epithelium, and delayed recovery of IL23R(-/-)Rag2(-/-) mice. This phenotype was rescued with exogenous IL22-Fc, and epithelial pSTAT3 was restored. Depletion of Thy1(+) innate lymphoid cells eliminated the majority of IL-22 production in the colon lamina propria of DSS-treated Rag2(-/-) mice, suggesting that these are the major IL-23 responsive innate cells in this context. In summary, we provide evidence for opposing consequences of IL-23R on innate and adaptive lymphoid cells in murine colitis.

journal_name

Mucosal Immunol

journal_title

Mucosal immunology

authors

Cox JH,Kljavin NM,Ota N,Leonard J,Roose-Girma M,Diehl L,Ouyang W,Ghilardi N

doi

10.1038/mi.2011.54

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

99-109

issue

1

eissn

1933-0219

issn

1935-3456

pii

mi201154

journal_volume

5

pub_type

杂志文章

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