Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Trends Endocrinol Metab. 2020 Jun;31(6):393-395. doi: 10.1016/j.tem.2020.04.001. Epub 2020 Apr 24.
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.
安吉阿里等人最近报道，TEPP-46 诱导 PKM2 四聚化，从而抑制其核易位，并抑制 CD4 T 细胞激活、辅助性 T 细胞（Th）1/Th17 细胞发育和实验性自身免疫性脑脊髓炎（EAE）的发展，无论是在体外还是体内。此外，TEPP-46 抑制 T 细胞糖酵解。这些发现确定了 PKM2 四聚化为潜在的治疗靶点。
