Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production of CCL17 (TARC), IL-5 and IL-13 in the lung. Mice treated with IL-22 before antigen challenge displayed reduced expression of CCL17 and IL-13 and significant amelioration of airway constriction and inflammation. We conclude that innate IL-22 limits airway inflammation, tissue damage and clinical decline in allergic lung disease.
Taube, C., Tertilt, C., Gyülveszi, G., Dehzad, N., Kreymborg, K., Schneeweiss, K., Michel, E., Reuter, S., Renauld, J.-C., Arnold-Schild, D., Schild, H., Buhl, R., & Becher, B. (2011). IL-22 Is Produced by Innate Lymphoid Cells and Limits Inflammation in Allergic Airway Disease. PLoS One, 6(7), e21799. https://doi.org/10.1371/journal.pone.0021799 (Original work published 2011)