Cutting Edge: Regulation of Intestinal Inflammation and Barrier Function by IL-17C

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  • Joseph M Reynolds
    Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center , Houston, TX 77054
  • Gustavo J Martinez
    Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center , Houston, TX 77054
  • Kalyan C Nallaparaju
    Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center , Houston, TX 77054
  • Seon Hee Chang
    Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center , Houston, TX 77054
  • Yi-Hong Wang
    Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center , Houston, TX 77054
  • Chen Dong
    Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center , Houston, TX 77054

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<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>

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