GATA3 induces the pathogenicity of Th17 cells via regulating GM-CSF expression.

ABSTRACT: T-bet-expressing Th17 (T-bet⁺RORγt⁺) cells are associated with the induction of pathology during experimental autoimmune encephalomyelitis (EAE) and the encephalitic nature of these Th17 cells can be explained by their ability to produce GM-CSF. However, the upstream regulatory mechanisms that control Csf2 (gene encoding GM-CSF) expression are still unclear. In this study, we found that Th17 cells dynamically expressed GATA3, the master transcription factor for Th2 cell differentiation, during their differentiation both in vitro and in vivo. Early deletion of Gata3 in three complimentary conditional knockout models by Cre-ERT2, hCd2 ^Cre and Tbx21 ^Cre, respectively, limited the pathogenicity of Th17 cells

SUBMITTER: Butcher MJ 

PROVIDER: S-EPMC10337884 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature