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. 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. For the development of effective drugs to target autoimmune neuroinflammation, much emphasis is placed on understanding the mechanisms underlying the differentiation and pathogenicity of Th17 cells. Continued investigation on the interplay of immune signals and metabolic cue and metabolic signatures of pathogenic Th17 cells will likely facilitate the development of novel therapeutic strategies to restore the dysregulated immune responses in MS.
Last date updated on June, 2014