NDLI: The Immunobiology of Colitis and Cholangitis in IL-23p19 and IL-17A Deleted dnTGFβRII Mice

Content Provider	PubMed Central
Author	Ando, Yugo Yang, Guo-xiang Tsuda, Masanobu Kawata, Kazuhito Zhang, Weici Nakajima, Takahiko Tsuneyama, Koichi Leung, Patrick Lian, Zhe-xiong Okazaki, Kazuichi Ridgway, William M. Norman, Gary L. Ansari, Aftab A. He, Xiao-song Coppel, Ross L. Gershwin, M. Eric
Abstract	dnTGFβRII mice, expressing a dominant negative form of TGFβ receptor II under control of the CD4 promoter, develop autoimmune colitis and cholangitis . We previously observed that deficiency in IL-12p40 led to a marked diminution of inflammation in both the colon and the liver. To distinguish whether IL-12p40 mediated protection acted via the IL-12 or IL-23 pathways, we generated an IL-23p19−/− dnTGFβRII strain deficient in IL-23 but not in IL-12; mice were longitudinally followed for changes in the natural history of disease and immune responses. Interestingly, IL-23p19−/− mice demonstrate dramatic improvement in their colitis but no changes in biliary pathology; mice also manifest reduced Th17 cell populations and unchanged IFN-γ levels. We submit that the IL-12/Th1 pathway is essential for biliary disease pathogenesis, while the IL-23/Th17 pathway mediates colitis. To further assess the mechanism of the IL-23 mediated protection from colitis, we generated an IL-17A−/− dnTGFβRII strain deficient in IL-17, a major effector cytokine produced by IL-23-dependent Th17 cells. Deletion of the IL-17A gene did not affect the severity of either cholangitis or colitis, suggesting that the IL-23/Th17 pathway contributes to the colon disease in an IL-17-independent manner. These results affirm that the IL-12/Th1 pathway is critical to biliary pathology in dnTGFβRII mice while the colitis is caused by a direct effect of IL-23.
Related Links	http://dx.doi.org/10.1002/hep.25803
Ending Page	1426
Page Count	9
Starting Page	1418
File Format	PDF
ISSN	02709139
e-ISSN	15273350
Journal	Hepatology (Baltimore, Md.)
Issue Number	4
Volume Number	56
Language	English
Publisher Date	2012-10-01
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Hepatology

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