ArticlePloS one2013
Type-I interferon is critical for FasL expression on lung cells to determine the severity of influenza.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Associations of three common polymorphisms in CD95 and CD95L promoter regions with gastric cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Pooled it
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- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
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- Efficacy and safety of asunercept, a CD95L-selective inhibitor, in hospitalised patients with moderate-to-severe COVID-19: ASUNCTIS, a multicentre, randomised, open-label, controlled, phase 2 trial.EClinicalMedicine · 2024Article
- Immunoregulatory Functions of Interferons During Genital HSV-2 Infection.Frontiers in immunology · 2021Review
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- The Role of Type I IFNs in Influenza: Antiviral Superheroes or Immunopathogenic Villains?Journal of innate immunity · 2020Review
- Evaluation of Activation and Inflammatory Activity of Myeloid Cells During Pathogenic Human Coronavirus Infection.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Programmed Cell Death in the Pathogenesis of Influenza.International journal of molecular sciences · 2018Review
- Overexpression of Chicken IRF7 Increased Viral Replication and Programmed Cell Death to the Avian Influenza Virus Infection Through TGF-Beta/FoxO Signaling Axis in DF-1.Frontiers in genetics · 2018Article
- Treating Influenza Infection, From Now and Into the Future.Frontiers in immunology · 2018Review
- The microbial metabolite desaminotyrosine protects from influenza through type I interferon.Science (New York, N.Y.) · 2017Article
- Death receptor 6 contributes to autoimmunity in lupus-prone mice.Nature communications · 2017Article
- The Impact of the Interferon/TNF-Related Apoptosis-Inducing Ligand Signaling Axis on Disease Progression in Respiratory Viral Infection and Beyond.Frontiers in immunology · 2017Review
- ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells.The Journal of veterinary medical science · 2016Article
- Type I IFN Does Not Promote Susceptibility to Foodborne Listeria monocytogenes.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice.Cell host & microbe · 2016Article
- Disease-promoting effects of type I interferons in viral, bacterial, and coinfections.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Review
- Type I interferons in infectious disease.Nature reviews. Immunology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of influenza A virus in mammals induces hyper lung pneumonia, which often causes lethal diseases. FasL is a specific ligand of Fas, which is a type-I transmembrane protein to induce cell death. Previously, it has been reported that the hyper induction of gene expression associated with Fas signal is observed in lethal influenza A virus infection. More importantly, it was also reported that functional mutation of the FasL gene protects the host against influenza A virus infection. These observations suggest that induction of FasL signal is functionally associated with the severity of influenza. However, regulation of the induction of FasL or Fas by influenza A virus infection is still unknown. Here, we demonstrated that FasL is induced after the viral infection, and inhibition of the Fas/FasL signal by treatment with a recombinant decoy receptor for FasL (Fas-Fc) increases the survival rate of mice after lethal infection of influenza A virus as well as functional mutation of the FasL gene in gld/gld mice. In addition, the induction level of FasL gene expression in the lung was correlated with the severity of influenza. We also showed that a variety of types of cells in the lung express FasL after the viral infection. Furthermore, type-I interferon induced by the viral infection was shown to be critical for induction of FasL protein expression in the lung. These findings suggested that expression of FasL protein induced by type-I IFN on the lung cell surface is critical to determine the severity of influenza.
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