1. IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease
- Author
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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; https://orcid.org/0000-0002-1541-7867, 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, and Becher, B; https://orcid.org/0000-0002-1541-7867
- Abstract
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.
- Published
- 2011