Abstract
IL-17-producing T(H)17 cells have been associated with autoimmune diseases such as multiple sclerosis (MS), psoriasis, Crohn's disease, and ulcerative colitis (Han et al., 2015), many of which lack effective therapies. Identifying effective approaches to selectively suppress T(H)17 cell development and function represents a legitimate strategy to cure these autoimmune disorders. T(H)17 cell differentiation requires rewiring of their metabolic program, transition from the oxidative phosphorylation-dominant catabolic phenotype in quiescent naïve T cells to glucose metabolism-orchestrated anabolic phenotype including lipogenesis. Here, we provide a focused review on the glycolytic-lipogenic pathway in T(H)17 development and pathogenicity. These studies reveal several metabolic checkpoints with specific regulation of T(H)17 cells (but not other T cell lineages), manifesting potential therapeutic opportunities to T(H)17 cell-mediated autoimmune diseases.