GPR65 promotes intestinal mucosal Th1 and Th17 cell differentiation and gut inflammation through downregulating NUAK2.

ABSTRACT: G protein-coupled receptor 65 (GPR65), a susceptibility gene for inflammatory bowel diseases (IBD), has been identified to promote Th17 cell pathogenicity and induce T cell apoptosis. However, the potential role of GPR65 in modulating CD4⁺ T cell immune responses in the pathogenesis of IBD stills not entirely understood. Here, we displayed that GPR65 expression was increased in inflamed intestinal mucosa of IBD patients and positively associated with disease activity. It was expressed in CD4⁺ T cells and robustly upregulated through the TNF-α-caspase 3/8 signalling pathway. Ectopic expression of GPR65 significantly promoted the differentiation of peripheral blood (PB) CD4⁺ T cells from IBD patients and HC to Th1 and Th17 cells in vitro. Importantly, conditi

SUBMITTER: Lin R 

PROVIDER: S-EPMC8958354 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature