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IL‐13Rα2 and IL‐10 coordinately suppress Th2‐dependent Inflammation and Immunopathology.

Immunopathology; such as airway hyper responsiveness (AHR) in asthmatics and fibrotic lesions following infection with Schistosoma sp. often result from excessive inflammation. However, the transition from inflammation to immunopathology is poorly understood. This study aimed to dissect critical mediators during Th2‐driven inflammation, following infection or airway allergen provocation, which mediate down‐stream pathology and to subsequently identify the regulatory mechanisms that control them. To separate inflammation from immunopathology, we used two in‐vivo models ‐ a model of asthma and Schistosomiasis, both of which present distinctive inflammation and downstream pathological changes. Following allergen challenge or infection, we observed an accumulation of IL‐10+ and Foxp3+ regulatory T cells (Treg) in the lungs or liver respectively. In the absence of IL‐10, Th2 inflammation was exacerbated, as well as the emergence of Th1 responses. Paradoxically, despite increased inflammation in IL‐10–/– mice pathology was curtailed. In both the lung and the liver, IL‐13R α 2, an endogenous neutralizer of IL‐13, was elevated. To test the role of IL‐13R α 2 in regulating Th2 pathology we generated mice deficient in both IL‐13R α 2 and IL‐10 (dKO). The absence of IL‐13R α 2, on an IL‐10–/– background, increased lung and liver pathology, compared to IL‐10–/– mice, indicating that IL‐13R α 2 is a key regulator of pathology, even during uncontrolled inflammation. This study presents a novel two‐pronged model of immunoregulation by IL‐10‐secreting Treg's and IL‐13R α 2, which could be exploited to control a variety of important Th2‐dominant diseases.