Journal
JOURNAL OF IMMUNOLOGY
Volume 189, Issue 9, Pages 4226-4230Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1103014
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Funding
- National Institutes of Health [AR050772, U19 AI071130]
- Cancer Prevention and Research Institute of Texas [RP120217]
- Crohn's and Colitis Foundation of America
- Leukemia and Lymphoma Society Scholar
- Olga and Harry Wiess Distinguished University Chair in Cancer Research at MD Anderson Cancer Center
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In the IL-17 family of cytokines, much is known about the sources and functions of IL-17, IL-17F, and IL-25 in the host defense against infection and in inflammatory diseases; however, the physiological function of IL-17C remains poorly understood. Using mice deficient in IL-17C, we demonstrate that this cytokine is crucial for the regulation of an acute experimental colitis elicited by dextran sulfate sodium. In this model, mice lacking IL-17C exhibited exacerbated disease that was associated with increased IL-17 expression by gamma delta T cells and Th17 cells. Moreover, IL-17C directly regulated the expression of the tight junction molecule occludin by colonic epithelial cells. Thus, our data suggest that IL-17C plays a critical role in maintaining mucosal barrier integrity. The Journal of Immunology, 2012, 189: 4226-4230.
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