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Opposing roles for IL‐13 and IL‐13 receptor α2 in health and disease

Summary:  Interleukin (IL)‐13 is a key inducer of several type‐2 cytokine‐dependent pathologies. It regulates inflammation, mucus production, tissue remodeling, and fibrosis. Consequently, it has become an important therapeutic target for a number of debilitating illnesses, including asthma, idiopathic pulmonary fibrosis, ulcerative colitis, as well as several other diseases in which IL‐13 is believed to be overproduced. In the murine model of schistosomiasis, IL‐13 has emerged as a central mediator of chronic infection‐induced liver pathology. Although IL‐4, IL‐5, IL‐10, and IL‐13 each regulate distinct aspects of the granulomatous inflammatory response, IL‐13 was identified as the primary mediator of liver fibrosis. Thus, elucidating the mechanisms that regulate the production and function of IL‐13 has become an intensive area of research. IL‐13 signaling is mediated by the type‐2 IL‐4 receptor, which consists of the IL‐4Rα and IL‐13Rα1 chains. However, another IL‐13‐binding chain, IL‐13Rα2, appears to strongly inhibit the activity of IL‐13. Animals deficient in IL‐13Rα2 fail to downmodulate granuloma formation in the chronic phase of infection. They also develop severe IL‐13‐dependent fibrosis and portal hypertension and quickly succumb to the infection. Here, we summarize findings from the schistosomiasis model, which illustrate opposing activities for IL‐13 and IL‐13Rα2 in health and disease.