A Compass to Guide Insights into TH17 Cellular Metabolism and Autoimmunity.

Adrianna N Wilson, Sarah A Mosure, Laura A Solt
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Abstract

T cells rapidly convert their cellular metabolic requirements upon activation, switching to a highly glycolytic program to satisfy their increasingly complex energy needs. Fundamental metabolic differences have been established for the development of Foxp3+ T regulatory (Treg) cells versus TH17 cells, alterations of which can drive disease. TH17 cell dysregulation is a driver of autoimmunity and chronic inflammation, contributing to pathogenesis in diseases such as multiple sclerosis. A recent paper published in Cell by Wagner, et al. combined scRNA-seq and metabolic mapping data to interrogate potential metabolic modulators of TH17 cell pathogenicity. This Compass to TH17 cell metabolism highlights the polyamine pathway as a critical regulator of TH17/Treg cell function, signifying its potential as a therapeutic target.

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指南洞察TH17细胞代谢和自身免疫的指南针。
T细胞在激活后迅速转换其细胞代谢需求,转换为高度糖酵解程序以满足其日益复杂的能量需求。Foxp3+ T调节(Treg)细胞与TH17细胞的发育已经建立了基本的代谢差异,其改变可以驱动疾病。TH17细胞失调是自身免疫和慢性炎症的驱动因素,有助于多发性硬化症等疾病的发病机制。Wagner等人最近在Cell上发表的一篇论文结合了scRNA-seq和代谢图谱数据,探究了TH17细胞致病性的潜在代谢调节剂。这种对TH17细胞代谢的指南针强调了多胺途径作为TH17/Treg细胞功能的关键调节因子,表明其作为治疗靶点的潜力。
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