Nur77 serves as a molecular brake of the metabolic switch during T cell activation to restrict autoimmunity.
Ontology highlight
ABSTRACT: T cells critically depend on reprogramming of metabolic signatures to meet the bioenergetic demands during activation and clonal expansion. Here we identify the transcription factor Nur77 as a cell-intrinsic modulator of T cell activation. Nur77-deficient T cells are highly proliferative, and lack of Nur77 is associated with enhanced T cell activation and increased susceptibility for T cell-mediated inflammatory diseases, such as CNS autoimmunity, allergic contact dermatitis and collagen-induced arthritis. Importantly, Nur77 serves as key regulator of energy metabolism in T cells, restricting mitochondrial respiration and glycolysis and controlling switching between different energy pathways. Transcriptional network analysis revealed that Nur77 modulates the expression of metabolic genes,
SUBMITTER: Liebmann M
PROVIDER: S-EPMC6112725 | biostudies-literature | 2018 Aug
REPOSITORIES: biostudies-literature
ACCESS DATA