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PLoS One. 2011;6(7):e21799. doi: 10.1371/journal.pone.0021799. Epub 2011 Jul 18.

IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease.

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1
III Medical Clinic, Johannes Gutenberg-University, Mainz, Germany.

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.

PMID:
21789181
PMCID:
PMC3138740
DOI:
10.1371/journal.pone.0021799
[Indexed for MEDLINE]
Free PMC Article
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