title: IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease.
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.
authors.affiliation: III Medical Clinic, Johannes Gutenberg-University, Mainz, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Taube
authors.forename: Christine
authors.initials: C
authors.lastname: Tertilt
authors.forename: Gabor
authors.initials: G
authors.lastname: Gyülveszi
authors.forename: Nina
authors.initials: N
authors.lastname: Dehzad
authors.forename: Katharina
authors.initials: K
authors.lastname: Kreymborg
authors.forename: Kristin
authors.initials: K
authors.lastname: Schneeweiss
authors.forename: Erich
authors.initials: E
authors.lastname: Michel
authors.forename: Sebastian
authors.initials: S
authors.lastname: Reuter
authors.forename: Jean-Christophe
authors.initials: JC
authors.lastname: Renauld
authors.forename: Danielle
authors.initials: D
authors.lastname: Arnold-Schild
authors.forename: Hansjörg
authors.initials: H
authors.lastname: Schild
authors.forename: Roland
authors.initials: R
authors.lastname: Buhl
authors.forename: Burkhard
authors.initials: B
authors.lastname: Becher
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D007113:Immunity, Innate / Q000187:drug effects / Q000276:immunology*; D007114:Immunization; D007136:Immunoglobulins / Q000097:blood; D007249:Inflammation / Q000097:blood / Q000150:complications* / Q000276:immunology* / Q000473:pathology; D018793:Interleukin-13 / Q000494:pharmacology; D007378:Interleukins / Q000008:administration & dosage / Q000096:biosynthesis* / Q000172:deficiency / Q000378:metabolism; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D010766:Phosphorylation / Q000187:drug effects; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000494:pharmacology; D012130:Respiratory Hypersensitivity / Q000097:blood / Q000150:complications* / Q000276:immunology*; D050796:STAT3 Transcription Factor / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D000097043:Interleukin-22
chemical_list: D000485:Allergens; D015415:Biomarkers; D007136:Immunoglobulins; D018793:Interleukin-13; D007378:Interleukins; D011994:Recombinant Proteins; D050796:STAT3 Transcription Factor; D014409:Tumor Necrosis Factor-alpha; D000097043:Interleukin-22; C494087:Stat3 protein, mouse