Kai Yang and Hongbo Chi
Multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system (CNS), results from
uncontrolled auto reactive T cells that infiltrate the CNS and attack the myelin sheath. Th17 cells play a prominent role
in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. Extensive
studies have focused on understanding the roles of cytokine signaling and transcriptional network in the differentiation
of Th17 cells and their pathogenicity in CNS inflammation. Aside from these events, activated T cells dynamically
reprogram their metabolic pathways to fulfill the bioenergic and biosynthetic requirements for proper T cell functions.
Emerging evidence indicates that modulation of these metabolic pathways impinges upon the differentiation of
Th17 cells and the pathogenesis of EAE. Thus, a better understanding of the functions and mechanisms of T cell
metabolism in Th17 cell biology may provide new avenues for therapeutic targeting of MS. In this review, we discuss
the recent advances in our understanding of T cell metabolic pathways involved in Th17 cell differentiation and CNS
inflammation.