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IL-22 Is Produced by Innate Lymphoid Cells and Limits Inflammation in Allergic Airway Disease.

Authors: Taube, C  Tertilt, C  Gyulveszi, G  Dehzad, N  Kreymborg, K  Schneeweiss, K  Michel, E  Reuter, S  Renauld, JC  Arnold-Schild, D  Schild, H  Buhl, R  Becher, B 
Citation: Taube C, etal., PLoS One. 2011;6(7):e21799. Epub 2011 Jul 18.
Pubmed: (View Article at PubMed) PMID:21789181
DOI: Full-text: DOI:10.1371/journal.pone.0021799

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.

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CRRD Object Information
CRRD ID: 5147401
Created: 2011-08-03
Species: All species
Last Modified: 2011-08-03
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.