PRMT1 Plays a Critical Role in Th17 Differentiation by Regulating Reciprocal Recruitment of STAT3 and STAT5.

ABSTRACT: Th17 cells are a class of Th cells that secrete IL-17 and mediate pathogenic immunity responsible for autoimmunity including experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis. Retinoic acid-related orphan receptor γ t (RORγt) is the critical transcription factor that controls the differentiation of Th17 cells. However, little is known about the transcriptional cofactors for RORγt in the regulation of Th17 differentiation. In this study, we demonstrate that protein arginine N-methyltransferase 1 (PRMT1) associates with RORγt and regulates mouse Th17 differentiation. Overexpression of PRMT1 promoted Th17 differentiation, whereas inactivation or knockdown of PRMT1 decreased Th17 differentiation while expanding Foxp3⁺ regulatory T cells. Consiste

SUBMITTER: Sen S 

PROVIDER: S-EPMC6039255 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature