Anti-IL-13Rα2 therapy promotes recovery in a murine model of inflammatory bowel disease.

摘要: There continues to be a major need for more effective inflammatory bowel disease (IBD) therapies. IL-13Rα2 is decoy receptor that binds the cytokine IL-13 with high affinity and diminishes its STAT6-mediated effector functions. Previously, we found was necessary IBD in mice deficient anti-inflammatory IL-10. Here, tested first time therapeutic antibody specifically targeting IL-13Rα2. We also used Il13ra2−/− dissect role of pathogenesis recovery. were modestly protected from induction dextran sodium sulfate (DSS)-induced colitis. Following 7-day recovery period, or wild-type administered IL-13Rα2-neutralizing had significantly improved colon health compared control mice. Neutralizing increase bioavailability promoted resolution even if neutralization occurred only during To link our observations large human cohort, conducted phenome-wide association study active variant (R130Q) has reduced Human subjects carrying R130Q reported lower risk Crohn’s disease. Our findings endorse moving anti-IL-13Rα2 into preclinical drug development goal accelerating maintaining remission patients.