| First Author | Taube C | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 7 | Pages | e21799 |
| PubMed ID | 21789181 | Mgi Jnum | J:175775 |
| Mgi Id | MGI:5287309 | Doi | 10.1371/journal.pone.0021799 |
| Citation | Taube C, et al. (2011) IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. PLoS One 6(7):e21799 |
| abstractText | 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. |
