Online now: Interleukin 23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity
How IL-23 drives an inflammatory Th17 cell state is poorly understood. Yang et al. identify two coordinated mechanisms specific to IL-23R signaling: the recruitment of CHD1 to stabilize RORγt expression and function and the blockade of glucocorticoid receptor function. Their study explains how IL-23 locks Th17 cells into an inflammatory disease-promoting state and provides a mechanism that explains steroid resistance in Th17 cells.
