ArticlePLoS pathogens2016
A20 Deficiency in Lung Epithelial Cells Protects against Influenza A Virus Infection.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 53 citations in OpenAlex.
- Exploring the role of the key gene TNFAIP3 between periodontitis and influenza A through bioinformatic analysis and molecular docking.PloS one · 2026Article
- The Dual Role of A20 (TNFAIP3) in Viral Infection: A Context-Dependent Regulator of Immunity and Pathogenesis.Viruses · 2025Review
- LMP7 as a Target for Coronavirus Therapy: Inhibition by Ixazomib and Interaction with SARS-CoV-2 Proteins Nsp13 and Nsp16.Pathogens (Basel, Switzerland) · 2025Article
- The Originally Established PBE Cell Line as a Reliable In Vitro Model for Investigating SIV Infection and Immunity.International journal of molecular sciences · 2025Article
- A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025Review
- Chronic exposure to low-level lipopolysaccharide dampens influenza-mediated inflammatory responseFrontiers in immunology · 2023Article
- Disease tolerance: a protective mechanism of lung infections.Frontiers in cellular and infection microbiology · 2023Review
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- IRF3 inhibits nuclear translocation of NF-κB to prevent viral inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Airway epithelial immunoproteasome subunit LMP7 protects against rhinovirus infection.Scientific reports · 2022Article
- Zinc and Respiratory Viral Infections: Important Trace Element in Anti-viral Response and Immune Regulation.Biological trace element research · 2022Review
- MicroRNA let-7 Suppresses Influenza A Virus Infection by Targeting RPS16 and Enhancing Type I Interferon Response.Frontiers in cellular and infection microbiology · 2022Article
- Article
- Review
- Airway epithelial cell necroptosis contributes to asthma exacerbation in a mouse model of house dust mite-induced allergic inflammation.Mucosal immunology · 2021Article
- Viral Respiratory Pathogens and Lung Injury.Clinical microbiology reviews · 2021Review
- C1qa deficiency in mice increases susceptibility to mouse hepatitis virus A59 infection.Journal of veterinary science · 2021Article
- NMP4 regulates the innate immune response to influenza A virus infection.Mucosal immunology · 2021Article
- Deficiency of eIF4B Increases Mouse Mortality and Impairs Antiviral Immunity.Frontiers in immunology · 2021Article
- Respiratory Epithelial Cells Respond toViruses · 2020Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A20 negatively regulates multiple inflammatory signalling pathways. We here addressed the role of A20 in club cells (also known as Clara cells) of the bronchial epithelium in their response to influenza A virus infection. Club cells provide a niche for influenza virus replication, but little is known about the functions of these cells in antiviral immunity. Using airway epithelial cell-specific A20 knockout (A20AEC-KO) mice, we show that A20 in club cells critically controls innate immune responses upon TNF or double stranded RNA stimulation. Surprisingly, A20AEC-KO mice are better protected against influenza A virus challenge than their wild type littermates. This phenotype is not due to decreased viral replication. Instead host innate and adaptive immune responses and lung damage are reduced in A20AEC-KO mice. These attenuated responses correlate with a dampened cytotoxic T cell (CTL) response at later stages during infection, indicating that A20AEC-KO mice are better equipped to tolerate Influenza A virus infection. Expression of the chemokine CCL2 (also named MCP-1) is particularly suppressed in the lungs of A20AEC-KO mice during later stages of infection. When A20AEC-KO mice were treated with recombinant CCL2 the protective effect was abrogated demonstrating the crucial contribution of this chemokine to the protection of A20AEC-KO mice to Influenza A virus infection. Taken together, we propose a mechanism of action by which A20 expression in club cells controls inflammation and antiviral CTL responses in response to influenza virus infection.
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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.