Abstract
Targeting glycolysis in T helper 17 (Th17) cells presents an attractive opportunity to treat Th17 cell-mediated autoimmune diseases such as multiple sclerosis (MS). Pyruvate kinase isoform 2 (PKM2) is a glycolytic enzyme expressed in T cells infiltrating the central nervous system in a mouse model of MS, suggesting PKM2 modulation could provide a new avenue for MS therapeutics. In a recent article in Science Signaling, Seki et al. show that pharmacological modulation of PKM2 alters but does not ameliorate disease in a mouse model of MS. These results warrant further consideration of PKM2 modulators to treat Th17 cell-mediated autoimmunity.
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