Abstract
Abstract IL-23 plays an essential role in TH17 cell-mediated cellular immunity and inflammation. However, the detailed mechanism remains elusive. In the current study, we found IL-23 activated the unfolded protein response (UPR) and promoted TH17 cell function. IL-23 induced UPR factor XBP1s and promotes its downstream genes in TH17 cells, leading to increased expression of TH17 cell cytokines. Induction of XBP1s required IRE1 activation by IL-23; pharmaceutical blockade of IRE1 largely diminished the effects of IL-23 on induction of TH17 cell effector cytokines. Taken together, our results suggest that IL-23 promotes TH17 cell function through activation of the UPR pathway. Targeting the IL-23-UPR axis may provide therapeutic benefit for TH17 cell-driven inflammatory and autoimmune diseases.
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