Abstract
Abstract Subsets of T helper cells are specialized for the production of specific cytokines, and this specificity is controlled by the function of transcription factors in each subset. Twist1, a basic helix-loop-helix (bHLH) transcription factor, is induced by STAT3-activating cytokines and inhibited by TGF-β in Th17 cells. Ectopic Twist1 expression in Th17 cells reduced IL-17A and IL-17F production while Twist1-deficient Th17 cells produced more IL-17A, IL-17F, and other inflammatory cytokines than wild type cells. In a myelin oligodendrocyte glycoprotein (MOGp35-55)-induced EAE disease model, Twist1-deficient mice manifest earlier onset of paralysis compared to wild type mice. Mechanistically, Twist1 controls cytokine production in Th17 cells by directly repressing Il6ra expression, limiting activation of the IL-6-STAT3 signaling pathway. Thus, Twist1 inhibits inflammatory cytokine production in Th17 cells, suggesting a central role for Twist1 in the regulatory network controlling autoimmune disease.
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