Viral recognition and type I interferon production by Toll-like receptor and an RNA helicase, RIG-I
Explore this paper's citation graph
Summary
It is found that RIG-I is essential for induction of type I interferons (IFNs) after infection with RNA viruses in fibroblasts and myeloid dendritic cells (DCs), and the TLR system exert antiviral responses in a cell type specific manner.
- Type
- article
- Published
- 2005-11-01
- Cited by
- 2
- References
- 24
- OpenAlex
- https://openalex.org/W2093608885
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:86769042
Keywords
IRF3, TRIF, TLR3, RIG-I, Biology
References
- Pattern recognition receptors TLR4 and CD14 mediate response to respiratory syncytial virus
- Plasmacytoid monocytes migrate to inflamed lymph nodes and produce large amounts of type I interferon
- The Roles of Toll-Like Receptor 9, MyD88, and DNA-Dependent Protein Kinase Catalytic Subunit in the Effects of Two Distinct CpG DNAs on Dendritic Cell Subsets1
- Species-Specific Recognition of Single-Stranded RNA via Toll-like Receptor 7 and 8
- Interferon-α induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6
- A FADD-dependent innate immune mechanism in mammalian cells
- Viral infection switches non-plasmacytoid dendritic cells into high interferon producers
- Herpes simplex virus type 1 activates murine natural interferon-producing cells through toll-like receptor 9.
- Innate Antiviral Responses by Means of TLR7-Mediated Recognition of Single-Stranded RNA
- Links between innate and adaptive immunity via type I interferon.
- Toll-like receptor signalling
- Role of a transductional-transcriptional processor complex involving MyD88 and IRF-7 in Toll-like receptor signaling.
- TLR9-dependent recognition of MCMV by IPC and DC generates coordinated cytokine responses that activate antiviral NK cell function.
- IRF3 and IRF7 Phosphorylation in Virus-infected Cells Does Not Require Double-stranded RNA-dependent Protein Kinase R or IκB Kinase but Is Blocked by Vaccinia Virus E3L Protein*
- Inferences, questions and possibilities in Toll-like receptor signalling
- Interferon-producing cells: on the front line in immune responses against pathogens.
- Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3
- The V proteins of paramyxoviruses bind the IFN-inducible RNA helicase, mda-5, and inhibit its activation of the IFN-beta promoter.
- Interleukin-1 receptor-associated kinase-1 plays an essential role for Toll-like receptor (TLR)7- and TLR9-mediated interferon-α induction
- Cell type-specific involvement of RIG-I in antiviral response.
Cited by
Related papers
- SARS‐CoV‐2 NSP8 suppresses type I and III IFN responses by modulating the RIG‐I/MDA5, TRIF, and STING signaling pathways
- Grass Carp Reovirus Nonstructural Proteins Avoid Host Antiviral Immune Response by Targeting the RLR Signaling Pathway
- EFTUD2 Is a Novel Innate Immune Regulator Restricting Hepatitis C Virus Infection through the RIG-I/MDA5 Pathway
- TRAF3IP3 negatively regulates type I interferon signaling by suppressing TBK1
- Research Progress on Antiviral Effect of MDA5 in Innate Immunity
- Porcine Respirovirus 1 Suppresses Host Type I Interferon Production and the JAK-STAT Signaling Pathway
- SARS‐CoV‐2 ORF9b antagonizes type I and III interferons by targeting multiple components of the RIG‐I/MDA‐5–MAVS, TLR3–TRIF, and cGAS–STING signaling pathways
- SARS-CoV-2 ORF9b Antagonizes Type I and III Interferons by Targeting Multiple Components of RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING Signaling Pathways
- Severe Acute Respiratory Syndrome Coronavirus M Protein Inhibits Type I Interferon Production by Impeding the Formation of TRAF3·TANK·TBK1/IKKϵ Complex*