揭示靶向糖酵解治疗Th17细胞介导的自身免疫性疾病的新挑战。
Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity.
作者信息
Mosure Sarah A, Solt Laura A
机构信息
Department of Immunology and Microbiology, The Scripps Research Institute, Jupiter, FL 33458, USA.
Department of Integrative Structural and Computational Biology, The Scripps Research Institute, Jupiter, FL 33458, USA.
出版信息
Immunometabolism. 2021;3(1). doi: 10.20900/immunometab20210006. Epub 2021 Jan 22.
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 , 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.
靶向辅助性T细胞17（Th17）细胞中的糖酵解过程为治疗诸如多发性硬化症（MS）等由Th17细胞介导的自身免疫性疾病提供了一个颇具吸引力的契机。丙酮酸激酶同工酶2（PKM2）是一种糖酵解酶，在MS小鼠模型中浸润中枢神经系统的T细胞中表达，这表明对PKM2的调节可能为MS治疗提供新途径。在最近发表于《 》的一篇文章中，关等学者表明，对PKM2进行药理调节会改变但不会改善MS小鼠模型中的疾病状况。这些结果值得进一步考虑将PKM2调节剂用于治疗Th17细胞介导的自身免疫性疾病。
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