ArticlePloS one2011
IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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Who cites it
69 citing papers in PubMed, 130 citations in OpenAlex.
- Contribution of Interleukin-22 Binding Protein to the Development of Allergen-Induced Airway Hyperresponsiveness.International journal of molecular sciences · 2026Article
- An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond.The American journal of pathology · 2026Review
- The interaction network between group 3 innate lymphoid cells and other cells.Fundamental research · 2025Review
- Baicalin restores innate lymphoid immune imbalance during exacerbation of COPD.Immunologic research · 2025Article
- Profile of immune response during nasal challenge with dermatophagoides pteronyssinus in subjects with allergic airway diseases.Journal of inflammation (London, England) · 2024Article
- Role of the type 3 cytokines IL-17 and IL-22 in modulating metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Review
- Intestinal Microbiota and Metabolomics Reveal the Role ofNutrients · 2023Article
- Protective and pathogenic functions of innate lymphoid cells in transplantation.Clinical and experimental immunology · 2023Review
- Crosstalk between the gut microbiota and innate lymphoid cells in intestinal mucosal immunity.Frontiers in immunology · 2023Review
- Role of Th17 Cytokines in Airway Remodeling in Asthma and Therapy Perspectives.Frontiers in allergy · 2022Review
- Systemic and local cytokine profile and risk factors for persistent allergic airway inflammation in patients sensitised to house dust mite allergens.BMC pulmonary medicine · 2021Article
- Innate lymphoid cells are double-edged swords under the mucosal barrier.Journal of cellular and molecular medicine · 2021Review
- Viral Respiratory Pathogens and Lung Injury.Clinical microbiology reviews · 2021Review
- The Anti-Inflammatory Effect of Aptamin C on House Dust Mite Extract-Induced Inflammation in Keratinocytes via Regulation of IL-22 and GDNF Production.Antioxidants (Basel, Switzerland) · 2021Article
- Role of IL-22 in persistent allergic airway diseases caused by house dust mite: a pilot study.BMC pulmonary medicine · 2021Article
- The Role of Group 3 Innate Lymphoid Cells in Lung Infection and Immunity.Frontiers in cellular and infection microbiology · 2021Review
- IL-22 is required for the induction of bronchus-associated lymphoid tissue in tolerant lung allografts.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Article
- ILC3 cells promote the proliferation and invasion of pancreatic cancer cells through IL-22/AKT signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Lower serum interleukin-22 and interleukin-35 levels are associated with disease status in neuromyelitis optica spectrum disorders.CNS neuroscience & therapeutics · 2020Article
- Synergy of Interleukin (IL)-5 and IL-18 in eosinophil mediated pathogenesis of allergic diseases.Cytokine & growth factor reviews · 2019Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.