ArticleJournal of virology2013
Interleukin-22 reduces lung inflammation during influenza A virus infection and protects against secondary bacterial infection.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 152 citations in OpenAlex.
- Review
- ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).International journal of molecular medicine · 2026Review
- IL-22 promotes the establishment of chronic gammaherpesvirus infection by supporting the germinal center response.PLoS pathogens · 2026Article
- Revisiting T cells: Innate actions and emerging links to innate memory response.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Trefoil factor 2 interacts with A4GNT to regulate inflammation to protect against pneumonia during influenza virus infection.iScience · 2025Article
- Article
- Age-Related Impairment of Innate and Adaptive Immune Responses Exacerbates Herpes Simplex Viral Infection.Pathogens (Basel, Switzerland) · 2025Article
- Post-viral lung diseases: the microbiota as a key player.ERJ open research · 2025Review
- Post-influenza bacterial infection: mechanisms of pathogenesis and advances in therapeutic strategies.Frontiers in microbiology · 2025Review
- I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024Review
- IL-22: A key inflammatory mediator as a biomarker and potential therapeutic target for lung cancer.Heliyon · 2024Review
- IL-22 Binding Protein Controls IL-22-Driven Bleomycin-Induced Lung Injury.The American journal of pathology · 2024Article
- Unraveling the dynamic mechanisms of natural killer cells in viral infections: insights and implications.Virology journal · 2024Review
- Interleukin-22 facilitates the interferon-λ-mediated production of tripartite motif protein 25 to inhibit replication of duck viral hepatitis A virus type 1.Veterinary research · 2023Article
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Influenza breakthrough infection in vaccinated mice is characterized by non-pathological lung eosinophilia.Frontiers in immunology · 2023Article
- Tissue-resident immunity in the lung: a first-line defense at the environmental interface.Seminars in immunopathology · 2022Review
- Article
- Respiratory Influenza Virus Infection Causes Dynamic Tuft Cell and Innate Lymphoid Cell Changes in the Small Intestine.Journal of virology · 2022Article
- Time-Dependent Increase in Susceptibility and Severity of Secondary Bacterial Infection during SARS-CoV-2 Infection.bioRxiv : the preprint server for biology · 2022Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-22 (IL-22) has redundant, protective, or pathogenic functions during autoimmune, inflammatory, and infectious diseases. Here, we addressed the potential role of IL-22 in host defense and pathogenesis during lethal and sublethal respiratory H3N2 influenza A virus (IAV) infection. We show that IL-22, as well as factors associated with its production, are expressed in the lung tissue during the early phases of IAV infection. Our data indicate that retinoic acid receptor-related orphan receptor-γt (RORγt)-positive αβ and γδ T cells, as well as innate lymphoid cells, expressed enhanced Il22 transcripts as early as 2 days postinfection. During lethal or sublethal IAV infections, endogenous IL-22 played no role in the control of IAV replication and in the development of the IAV-specific CD8(+) T cell response. During lethal infection, where wild-type (WT) mice succumbed to severe pneumonia, the lack of IL-22 did not accelerate or delay IAV-associated pathogenesis and animal death. In stark contrast, during sublethal IAV infection, IL-22-deficient animals had enhanced lung injuries and showed a lower airway epithelial integrity relative to WT littermates. Of importance, the protective effect of endogenous IL-22 in pulmonary damages was associated with a more controlled secondary bacterial infection. Indeed, after challenge with Streptococcus pneumoniae, IAV-experienced Il22(-/-) animals were more susceptible than WT controls in terms of survival rate and bacterial burden in the lungs. Together, IL-22 plays no major role during lethal influenza but is beneficial during sublethal H3N2 IAV infection, where it limits lung inflammation and subsequent bacterial superinfections.
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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.