Id2 acts as a metabolic checkpoint underpinning Th17 cell fate decision [RNA-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. RNA-sequencing of CD4+YFP+ cells from spleen and lymph node in Il17CreR26YFP, Il17CreR26YFP Id2f/f and Il17CreR26YFP Id2f/f E2Af/f HEBf/f mice; or CD4+YFP+SLAMF6+ and CD4+YFP+CXCR6+ cells from Il17CreR26YFP mice.