ArticleThe Journal of biological chemistry2012
Interleukin-22 is produced by invariant natural killer T lymphocytes during influenza A virus infection: potential role in protection against lung epithelial damages.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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Who cites it
119 citing papers in PubMed, 173 citations in OpenAlex.
- E protein-driven iNKT subset modulation shapes early immune responses during influenza A virus infection.American journal of respiratory cell and molecular biology · 2026Article
- Accumulation of Quinolinic Acid Modulates the Pulmonary Immune Response During Influenza Infection.International journal of tryptophan research : IJTR · 2026Article
- Single-cell antigen receptor sequencing in pigs with influenza.Communications biology · 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
- Influence of Donor-Specific Characteristics on Cytokine Responses in H3N2 Influenza A Virus Infection: New Insights from an Ex Vivo Model.International journal of molecular sciences · 2024Article
- The surveillance of viral infections by the unconventional Type I NKT cell.Frontiers in immunology · 2024Review
- From Snoot to Tail: A Brief Review of Influenza Virus Infection and Immunity in Pigs.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Aging unconventionally: γδ T cells, iNKT cells, and MAIT cells in aging.Seminars in immunology · 2023Review
- Invariant natural killer T cells in lung diseases.Experimental & molecular medicine · 2023Review
- Advances in immune response to pulmonary infection: Nonspecificity, specificity and memory.Chronic diseases and translational medicine · 2023Review
- Vunakizumab-IL22, a Novel Fusion Protein, Promotes Intestinal Epithelial Repair and Protects against Gut Injury Induced by the Influenza Virus.Biomedicines · 2023Article
- Profiling of innate and adaptive immune cells during influenza virus infection reveals sex bias in invariant natural killer T (iNKT) cells.Immunity, inflammation and disease · 2023Article
- Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023Review
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Tissue resident iNKT17 cells facilitate cancer cell extravasation in liver metastasis via interleukin-22.Immunity · 2023Article
- Review
- Article
- Nanovaccines against Viral Infectious Diseases.Pharmaceutics · 2022Review
- Development of off-the-shelf hematopoietic stem cell-engineered invariant natural killer T cells for COVID-19 therapeutic intervention.Stem cell research & therapy · 2022Article
59 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invariant natural killer T (iNKT) cells are non-conventional lipid-reactive αβ T lymphocytes that play a key role in host responses during viral infections, in particular through the swift production of cytokines. Their beneficial role during experimental influenza A virus (IAV) infection has recently been proposed, although the mechanisms involved remain elusive. Here we show that during in vivo IAV infection, mouse pulmonary iNKT cells produce IFN-γ and IL-22, a Th17-related cytokine critical in mucosal immunity. Although permissive to viral replication, IL-22 production by iNKT cells is not due to IAV infection per se of these cells but is indirectly mediated by IAV-infected dendritic cells (DCs). We show that activation of the viral RNA sensors TLR7 and RIG-I in DCs is important for triggering IL-22 secretion by iNKT cells, whereas the NOD-like receptors NOD2 and NLRP3 are dispensable. Invariant NKT cells respond to IL-1β and IL-23 provided by infected DCs independently of the CD1d molecule to release IL-22. In vitro, IL-22 protects IAV-infected airway epithelial cells against mortality but has no role on viral replication. Finally, during early IAV infection, IL-22 plays a positive role in the control of lung epithelial damages. Overall, IAV infection of DCs activates iNKT cells, providing a rapid source of IL-22 that might be beneficial to preserve the lung epithelium integrity.
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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.