ArticlePLoS pathogens2013
Type I IFN triggers RIG-I/TLR3/NLRP3-dependent inflammasome activation in influenza A virus infected cells.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
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Who cites it
153 citing papers in PubMed.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- PANoptosis as a Therapeutic Target for COVID-19.Current microbiology · 2026Review
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- Development of rapid multiplex human herpesvirus detection systems based on recombinase polymerase amplification and a lateral flow assay.Frontiers in cell and developmental biology · 2026Article
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- IncRNA IPAN antagonizes RIG-I/TRIM25-mediated degradation of influenza A virus PB1 to promote viral replication.Biosafety and health · 2025Article
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Understanding the Molecular Interactions Between Influenza A Virus andPathogens (Basel, Switzerland) · 2025Article
- Leveraging a comprehensive unbiased RNAseq database to characterize human monocyte-derived macrophage gene expression profiles within commonly employed in vitro polarization methods.Scientific reports · 2024Article
- The assembly of neutrophil inflammasomes during COVID-19 is mediated by type I interferons.PLoS pathogens · 2024Article
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.International journal of molecular sciences · 2024Review
- NLRP3 Inflammasome Involvement in Heart, Liver, and Lung Diseases-A Lesson from Cytokine Storm Syndrome.International journal of molecular sciences · 2023Review
- New Potentiality of Bioactive Substances: Regulating the NLRP3 Inflammasome in Autoimmune Diseases.Nutrients · 2023Review
- PANoptosis: Mechanism and Role in Pulmonary Diseases.International journal of molecular sciences · 2023Review
- Posttranslational ISGylation of NLRP3 by HERC enzymes facilitates inflammasome activation in models of inflammation.The Journal of clinical investigation · 2023Article
- Structural Investigations of Interactions between the Influenza a Virus NS1 and Host Cellular Proteins.Viruses · 2023Review
- The NLRP3 inflammasome in viral infection (Review).Molecular medicine reports · 2023Review
- Review
93 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Influenza A virus (IAV) triggers a contagious and potentially lethal respiratory disease. A protective IL-1β response is mediated by innate receptors in macrophages and lung epithelial cells. NLRP3 is crucial in macrophages; however, which sensors elicit IL-1β secretion in lung epithelial cells remains undetermined. Here, we describe for the first time the relative roles of the host innate receptors RIG-I (DDX58), TLR3, and NLRP3 in the IL-1β response to IAV in primary lung epithelial cells. To activate IL-1β secretion, these cells employ partially redundant recognition mechanisms that differ from those described in macrophages. RIG-I had the strongest effect through a MAVS/TRIM25/Riplet-dependent type I IFN signaling pathway upstream of TLR3 and NLRP3. Notably, RIG-I also activated the inflammasome through interaction with caspase 1 and ASC in primary lung epithelial cells. Thus, NS1, an influenza virulence factor that inhibits the RIG-I/type I IFN pathway, strongly modulated the IL-1β response in lung epithelial cells and in ferrets. The NS1 protein derived from a highly pathogenic strain resulted in increased interaction with RIG-I and inhibited type I IFN and IL-1β responses compared to the least pathogenic virus strains. These findings demonstrate that in IAV-infected lung epithelial cells RIG-I activates the inflammasome both directly and through a type I IFN positive feedback loop.
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