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10.1016/j.immuni.2015.09.003

http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.09.003
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C6044435!6044435!26431948
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suck abstract from ncbi


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pmid26431948      Immunity 2015 ; 43 (4): 727-38
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  • IL-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability #MMPMID26431948
  • Lee JS; Tato CM; Joyce-Shaikh B; Gulan F; Cayatte C; Chen Y; Blumenschein WM; Judo M; Chen K; Ayanoglu G; McClanahan TK; Li X; Cua DJ
  • Immunity 2015[Oct]; 43 (4): 727-38 PMID26431948show ga
  • Whether IL-17A has pathogenic and/or protective roles in the gut mucosa is controversial and few studies have analyzed specific cell populations for protective functions within the inflamed colonic tissue. Here we provide evidence for IL-17A dependent regulation of the tight junction protein occludin during epithelial injury that limits excessive permeability and maintains barrier integrity. Analysis of epithelial cells showed that in the absence of Act-1 signaling, the protective effect of IL-17A was abrogated and inflammation was enhanced. We demonstrate that following acute intestinal injury, IL-23R+ ROR?t+ ?? T cells in the colonic lamina propria are the primary producers of early, gut-protective IL-17A, over other cell populations such as memory Th17 cells and ILC3. This production of IL-17A was IL-23 independent, leaving protective IL-17 intact in the absence of IL-23. These results suggest that IL-17 producing resident ?? T cells are important for the maintenance, and protectionof epithelial barriers in the intestinal mucosa.
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