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10.1038/ncomms11627

http://scihub22266oqcxt.onion/10.1038/ncomms11627
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C4874038!4874038!27193261
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suck abstract from ncbi


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pmid27193261      Nat+Commun 2016 ; 7 (ä): ä
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  • T-bet is a key modulator of IL-23-driven pathogenic CD4+ T cell responses in the intestine #MMPMID27193261
  • Krausgruber T; Schiering C; Adelmann K; Harrison OJ; Chomka A; Pearson C; Ahern PP; Shale M; Oukka M; Powrie F
  • Nat Commun 2016[]; 7 (ä): ä PMID27193261show ga
  • IL-23 is a key driver of pathogenic Th17 cell responses. It has been suggested that the transcription factor T-bet is required to facilitate IL-23-driven pathogenic effector functions; however, the precise role of T-bet in intestinal T cell responses remains elusive. Here, we show that T-bet expression by T cells is not required for the induction of colitis or the differentiation of pathogenic Th17 cells but modifies qualitative features of the IL-23-driven colitogenic response by negatively regulating IL-23R expression. Consequently, absence of T-bet leads to unrestrained Th17 cell differentiation and activation characterized by high amounts of IL-17A and IL-22. The combined increase in IL-17A/IL-22 results in enhanced epithelial cell activation and inhibition of either IL-17A or IL-22 leads to disease amelioration. Our study identifies T-bet as a key modulator of IL-23-driven colitogenic responses in the intestine and has important implications for understanding of heterogeneity among inflammatory bowel disease patients.
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