STING is an intrinsic checkpoint inhibitor that restrains the TH17 cell pathogenic program.
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ABSTRACT: External and intrinsic factors regulate the transcriptional profile of T helper 17 (TH17) cells, thereby affecting their pathogenic potential and revealing their context-dependent plasticity. The stimulator of interferon genes (STING), a component of the intracellular DNA-sensing pathway, triggers immune responses but remains largely unexplored in T cells. Here, we describe an intrinsic role of STING in limiting the TH17 cell pathogenic program. We demonstrate that non-pathogenic TH17 cells express higher levels of STING than those activated under pathogenic conditions. Activation of STING induces interleukin-10 (IL-10) production in TH17 cells, decreasing IL-17A and IL-23R expression in a type I interferon (IFN)-independent manner. Mechanistical
SUBMITTER: Damasceno LEA
PROVIDER: S-EPMC9188824 | biostudies-literature | 2022 May
REPOSITORIES: biostudies-literature
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