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HIF-1 in T cells ameliorated dextran sodium sulfate-induced murine colitis. | LitMetric

AI Article Synopsis

  • * Studies showed that HIF-1 is present in T cells within inflamed colonic tissue, indicating its involvement in IBD development.
  • * Experiments suggest that HIF-1 helps maintain a balance between regulatory T cells (Tregs) and effector T cells (Teffs), and enhancing HIF-1 could be a potential treatment strategy for managing IBD.

Article Abstract

HIF-1 is active in hypoxia, such as inflamed mucosa, and HIF-1 in epithelium has been reported to control inflamed mucosa in IBD models. Although T cells play an important role for pathogenesis of IBD, the function of HIF-1 in T cells remains to be elucidated. We aimed to clarify the function of HIF-1 in T cells in IBD with focus on the balance between Treg and Teff. Double immunohistochemistry of colonic mucosa in IBD patients showed that HIF-1 was expressed in T cells infiltrating the inflamed mucosa, suggesting that HIF-1 in T cells is involved in the pathogenesis. DSS administration to T cell-specific HIF-1α KO mice showed more severe colonic inflammation than control mice with the up-regulation of Th1 and Th17. Hypoxic stimulation in vitro increased Treg activation in WT T cells but not in HIF-1-deleted T cells. In contrast, hypoxic stimulation increased Th17 activation, and the degree was higher in HIF-1-deleted cells than in control cells. These results show that hypoxia controls intestinal inflammation by regulating cytokine balance in a HIF-1-dependent manner, suggesting that strengthening HIF-1 induction in T cells at the sites of inflammation might be a therapeutic strategy for IBD regulation.

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Source
http://dx.doi.org/10.1189/jlb.1011518DOI Listing

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