PRC1 promotes immunosuppressive macrophages in sepsis via β-catenin/STAT3 signaling

Our data demonstrated that PRC1 is upregulated in endotoxin-tolerant macrophages, and that increased PRC1 expression maintains STAT3 activation via a β-catenin-dependent mechanism and impairs inflammatory response of macrophages during septic immunosuppression. Targeting PRC1/β-catenin/ STAT3 could represent a novel strategy for the management of septic immunosuppression and restore the inflammatory response of endotoxin-tolerant macrophages.