实验性自身免疫性脑脊髓炎
T细胞
体内
巴基斯坦卢比
糖酵解
细胞
化学
染色体易位
脑脊髓炎
细胞生物学
体外
细胞生长
生物
癌症研究
免疫学
生物化学
多发性硬化
免疫系统
丙酮酸激酶
新陈代谢
遗传学
基因
标识
DOI:10.1016/j.tem.2020.04.001
摘要
Angiari et al. recently reported that TEPP-46 induces PKM2 tetramerization, thereby inhibiting its nuclear translocation and suppressing CD4+ T cell activation, T helper (Th)1/Th17 cell development, and experimental autoimmune encephalomyelitis (EAE) development both in vitro and in vivo. Moreover, TEPP-46 suppresses T cell glycolysis. These findings identify PKM2 tetramerization as a potential therapeutic target. Angiari et al. recently reported that TEPP-46 induces PKM2 tetramerization, thereby inhibiting its nuclear translocation and suppressing CD4+ T cell activation, T helper (Th)1/Th17 cell development, and experimental autoimmune encephalomyelitis (EAE) development both in vitro and in vivo. Moreover, TEPP-46 suppresses T cell glycolysis. These findings identify PKM2 tetramerization as a potential therapeutic target.
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