A Compass to Guide Insights into T(H)17 Cellular Metabolism and Autoimmunity

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 T(H)17 cells, alterations of which can drive disease. T(H)17 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 T(H)17 cell pathogenicity. This Compass to T(H)17 cell metabolism highlights the polyamine pathway as a critical regulator of T(H)17/Treg cell function, signifying its potential as a therapeutic target.