Interleukin 23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity - PubMed
3 hours ago
- #IL-23
- #Autoimmunity
- #Th17 cells
- IL-23R signaling is crucial for pro-inflammatory Th17 cells in autoimmune inflammation.
- IL-23 specifically promotes CHD1-STAT3 interaction and binding at RORγt locus to enforce Th17 state.
- IL-23 alters glucocorticoid receptor phosphorylation, preventing its activation and anti-inflammatory function.
- These mechanisms identify potential therapeutic targets for Th17-driven autoimmune diseases.
- The study integrates phosphoproteomic and transcriptomic data to differentiate IL-23 from IL-12 signaling.