Id2 acts as a metabolic checkpoint underpinning Th17 cell fate decision [scRNA-seq]
T helper 17 (Th17) cells protect barrier tissues but also trigger autoimmunity.  The precise mechanisms control these opposing processes remain unclear. We identify Id2 as a key factor for pathogenic Th17 cells. Id2 expression is markedly elevated in Myelin-reactive T cells from multiple sclerosis (MS) patients and autoimmune mice. Mice lacking Id2 in Th17 cells completely fail to develop neuroinflammation and do not generate neuron-pathogenic Th17 subset. Overall design: Single Cell analysis of CD4+YFP+ cells from spleen in Id2 deficient and wild type cells.