IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease.
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...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2011-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3138740?pdf=render |
| _version_ | 1811259665486446592 |
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| author | Christian Taube Christine Tertilt Gabor Gyülveszi Nina Dehzad Katharina Kreymborg Kristin Schneeweiss Erich Michel Sebastian Reuter Jean-Christophe Renauld Danielle Arnold-Schild Hansjörg Schild Roland Buhl Burkhard Becher |
| author_facet | Christian Taube Christine Tertilt Gabor Gyülveszi Nina Dehzad Katharina Kreymborg Kristin Schneeweiss Erich Michel Sebastian Reuter Jean-Christophe Renauld Danielle Arnold-Schild Hansjörg Schild Roland Buhl Burkhard Becher |
| author_sort | Christian Taube |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-12T18:34:57Z |
| format | Article |
| id | doaj.art-85a04ec9fb114ed1b21edbb64297cbef |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-12T18:34:57Z |
| publishDate | 2011-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-85a04ec9fb114ed1b21edbb64297cbef2022-12-22T03:20:57ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0167e2179910.1371/journal.pone.0021799IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease.Christian TaubeChristine TertiltGabor GyülvesziNina DehzadKatharina KreymborgKristin SchneeweissErich MichelSebastian ReuterJean-Christophe RenauldDanielle Arnold-SchildHansjörg SchildRoland BuhlBurkhard BecherInterleukin (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.http://europepmc.org/articles/PMC3138740?pdf=render |
| spellingShingle | Christian Taube Christine Tertilt Gabor Gyülveszi Nina Dehzad Katharina Kreymborg Kristin Schneeweiss Erich Michel Sebastian Reuter Jean-Christophe Renauld Danielle Arnold-Schild Hansjörg Schild Roland Buhl Burkhard Becher IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. PLoS ONE |
| title | IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. |
| title_full | IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. |
| title_fullStr | IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. |
| title_full_unstemmed | IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. |
| title_short | IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease. |
| title_sort | il 22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease |
| url | http://europepmc.org/articles/PMC3138740?pdf=render |
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