ArticleMucosal immunology2020
Targeting the IL-22/IL-22BP axis enhances tight junctions and reduces inflammation during influenza infection.
Article in Mucosal immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Respiratory mucosal immunity: Biological functions, diseases, prevention and therapy.Genes & diseases · 2026Review
- Contribution of Interleukin-22 Binding Protein to the Development of Allergen-Induced Airway Hyperresponsiveness.International journal of molecular sciences · 2026Article
- Interleukin-23 in lung and airway diseases: from pathogenesis to precision-guided therapeutic targeting.Frontiers in pharmacology · 2026Review
- Characterization of subchronic lung and brain consequences caused by mouse-adapted SARS-CoV-2 and influenza A infection of C57BL6 mice.Frontiers in immunology · 2026Article
- Interleukin-10 family cytokines: key regulators and novel therapeutic targets for respiratory diseases.Inflammopharmacology · 2025Review
- I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024Review
- Review of the potential value of serum interleukin levels as prognostic biomarkers of liver failure.World journal of clinical cases · 2024Review
- Gut microbiota-derived acetate attenuates lung injury induced by influenza infection via protecting airway tight junctions.Journal of translational medicine · 2024Article
- IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The role of Interleukin-22 in severe acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- IL-22 Binding Protein Controls IL-22-Driven Bleomycin-Induced Lung Injury.The American journal of pathology · 2024Article
- Epithelial plasticity and innate immune activation promote lung tissue remodeling following respiratory viral infection.Nature communications · 2023Article
- IL-22 Is Deleterious along with IL-17 in Allergic Asthma but Is Not Detrimental in the Comorbidity Asthma and Acute Pneumonia.International journal of molecular sciences · 2023Article
- Role of IL-22 in intestinal microenvironment and potential targeted therapy through diet.Immunologic research · 2023Review
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Zonula Occludens Proteins Signaling in Inflammation and Tumorigenesis.International journal of biological sciences · 2023Review
- Disease tolerance: a protective mechanism of lung infections.Frontiers in cellular and infection microbiology · 2023Review
- Proteomic aptamer analysis reveals serum biomarkers associated with disease mechanisms and phenotypes of systemic sclerosis.Frontiers in immunology · 2023Article
- Article
- Bona Fide Th17 Cells without Th1 Functional Plasticity Protect against Influenza.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The seasonal burden of influenza coupled with the pandemic outbreaks of more pathogenic strains underscore a critical need to understand the pathophysiology of influenza injury in the lung. Interleukin-22 (IL-22) is a promising cytokine that is critical in protecting the lung during infection. This cytokine is strongly regulated by the soluble receptor IL-22-binding protein (IL-22BP), which is constitutively expressed in the lungs where it inhibits IL-22 activity. The IL-22/IL-22BP axis is thought to prevent chronic exposure of epithelial cells to IL-22. However, the importance of this axis is not understood during an infection such as influenza. Here we demonstrate through the use of IL-22BP-knockout mice (il-22ra2
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31597930PMC6917921W2979939952What OpenQuestion holds
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.