ArticlePLoS pathogens2012
A20 (Tnfaip3) deficiency in myeloid cells protects against influenza A virus infection.
Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed.
- Investigating the Role of A20 in Respiratory Syncytial Virus Immunopathogenesis in a BALB/c Mouse Model.Immunity, inflammation and disease · 2026Article
- Article
- The Dual Role of A20 (TNFAIP3) in Viral Infection: A Context-Dependent Regulator of Immunity and Pathogenesis.Viruses · 2025Review
- Article
- A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025Review
- Myeloid A20 is critical for alternative macrophage polarization and type-2 immune-mediated helminth resistance.Frontiers in immunology · 2024Article
- Chronic exposure to low-level lipopolysaccharide dampens influenza-mediated inflammatory responseFrontiers in immunology · 2023Article
- Ubiquitin-binding domain in ABIN1 is critical for regulating cell death and inflammation during development.Cell death and differentiation · 2022Article
- Article
- 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
- Identification of Nifurtimox and Chrysin as Anti-Influenza Virus Agents by Clinical Transcriptome Signature Reversion.International journal of molecular sciences · 2022Article
- Neutrophil DREAM promotes neutrophil recruitment in vascular inflammation.The Journal of experimental medicine · 2022Article
- MicroRNA let-7 Suppresses Influenza A Virus Infection by Targeting RPS16 and Enhancing Type I Interferon Response.Frontiers in cellular and infection microbiology · 2022Article
- Comparison of Transcriptomic Signatures between Monkeypox-Infected Monkey and Human Cell Lines.Journal of immunology research · 2022Article
- A Previously Undiscovered Circular RNA, circTNFAIP3, and Its Role in Coronavirus Replication.mBio · 2021Article
- Zinc is an important inter-kingdom signal between the host and microbe.Veterinary research · 2021Review
- Cellular Deubiquitylating Enzyme: A Regulatory Factor of Antiviral Innate Immunity.Frontiers in microbiology · 2021Review
- Potential Molecular Mechanisms and Remdesivir Treatment for Acute Respiratory Syndrome Corona Virus 2 Infection/COVID 19 Through RNA Sequencing and Bioinformatics Analysis.Bioinformatics and biology insights · 2021Article
- Deficiency of eIF4B Increases Mouse Mortality and Impairs Antiviral Immunity.Frontiers in immunology · 2021Article
- Investigating Ketone Bodies as Immunometabolic Countermeasures against Respiratory Viral Infections.Med (New York, N.Y.) · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune response provides the first line of defense against viruses and other pathogens by responding to specific microbial molecules. Influenza A virus (IAV) produces double-stranded RNA as an intermediate during the replication life cycle, which activates the intracellular pathogen recognition receptor RIG-I and induces the production of proinflammatory cytokines and antiviral interferon. Understanding the mechanisms that regulate innate immune responses to IAV and other viruses is of key importance to develop novel therapeutic strategies. Here we used myeloid cell specific A20 knockout mice to examine the role of the ubiquitin-editing protein A20 in the response of myeloid cells to IAV infection. A20 deficient macrophages were hyperresponsive to double stranded RNA and IAV infection, as illustrated by enhanced NF-κB and IRF3 activation, concomitant with increased production of proinflammatory cytokines, chemokines and type I interferon. In vivo this was associated with an increased number of alveolar macrophages and neutrophils in the lungs of IAV infected mice. Surprisingly, myeloid cell specific A20 knockout mice are protected against lethal IAV infection. These results challenge the general belief that an excessive host proinflammatory response is associated with IAV-induced lethality, and suggest that under certain conditions inhibition of A20 might be of interest in the management of IAV infections.
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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.