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- Joseph M. Reynolds
- Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054
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- Gustavo J. Martinez
- Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054
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- Kalyan C. Nallaparaju
- Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054
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- Seon Hee Chang
- Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054
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- Yi-Hong Wang
- Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054
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- Chen Dong
- Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054
説明
<jats:title>Abstract</jats:title> <jats:p>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 γδ 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.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 189 (9), 4226-4230, 2012-11-01
The American Association of Immunologists