Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity.

Immunometabolism Pub Date : 2021-01-01 Epub Date: 2021-01-22 DOI:10.20900/immunometab20210006
Sarah A Mosure, Laura A Solt
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引用次数: 2

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.

Abstract Image

靶向糖酵解治疗Th17细胞介导的自身免疫的新挑战
靶向T辅助17 (Th17)细胞的糖酵解为治疗Th17细胞介导的自身免疫性疾病(如多发性硬化症(MS))提供了一个有吸引力的机会。丙酮酸激酶异构体2 (Pyruvate kinase isoform 2, PKM2)是一种在MS小鼠模型中浸润中枢神经系统的T细胞中表达的糖酵解酶,这表明PKM2的调节可能为MS的治疗提供新的途径。在Science Signaling最近的一篇文章中,Seki等人表明,在ms小鼠模型中,PKM2的药理学调节改变了但并没有改善疾病。这些结果值得进一步考虑PKM2调节剂来治疗Th17细胞介导的自身免疫。
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