ArticleJournal of virology2013
Rabies virus is recognized by the NLRP3 inflammasome and activates interleukin-1β release in murine dendritic cells.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- A comparative analysis of the dendritic cell response upon exposure to different rabies virus strains.PLoS neglected tropical diseases · 2025Article
- Immunological findings of West Caucasian bat virus in an accidental host.Journal of virology · 2025Article
- Infectious bronchitis-virus-like QX strain transmission, pathogenesis, replication, and host miRNA biogenesis pathway hijacking mechanism.Frontiers in cellular and infection microbiology · 2025Article
- The Interplay Between Viral Infection and Cell Death: A Ping-Pong Effect.Advances in virology · 2025Review
- Inflammasome activation by viral infection: mechanisms of activation and regulation.Frontiers in microbiology · 2023Review
- Article
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis.Viruses · 2022Review
- Interplay between hypoxia and inflammation contributes to the progression and severity of respiratory viral diseases.Molecular aspects of medicine · 2021Review
- Protective effects of the NLRP3 inflammasome against infectious bursal disease virus replication in DF-1 cells.Archives of virology · 2021Article
- STING promotes NLRP3 localization in ER and facilitates NLRP3 deubiquitination to activate the inflammasome upon HSV-1 infection.PLoS pathogens · 2020Article
- Article
- Human metapneumovirus activates NOD-like receptor protein 3 inflammasome via its small hydrophobic protein which plays a detrimental role during infection in mice.PLoS pathogens · 2019Article
- Cytosolic Recognition of Microbes and Pathogens: Inflammasomes in Action.Microbiology and molecular biology reviews : MMBR · 2018Review
- HSP60 critically regulates endogenous IL-1β production in activated microglia by stimulating NLRP3 inflammasome pathway.Journal of neuroinflammation · 2018Article
- Intracellular Antiviral Immunity.Advances in virus research · 2018Review
- Impact of caspase-1/11, -3, -7, or IL-1Cell death discovery · 2017Article
- EV71 3D Protein Binds with NLRP3 and Enhances the Assembly of Inflammasome Complex.PLoS pathogens · 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
- Inflammasomes and its importance in viral infections.Immunologic research · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Inflammasome activation is important for the development of an effective host defense against many pathogens, including RNA viruses. However, the mechanism by which the inflammasome recognizes RNA viruses and its role in rabies virus (RABV) pathogenicity and immunogenicity remain poorly defined. To determine the function of the inflammasome in response to RABV infection, we infected murine bone marrow-derived dendritic cells (BMDCs) with RABV. Our results indicate that the infection of BMDCs with RABV induces both the production of pro-interleukin-1β (pro-IL-1β) and its processing, resulting in the secretion of active IL-1β through activation of the NLRP3-, ASC-, and caspase-1-dependent inflammasome. As previously shown for the induction of type I interferon by RABV, the induction of pro-IL-1β also depends upon IPS-1. We demonstrate that both the production of pro-IL-1β and activation of the inflammasome require viral replication. We also demonstrate that increased viral replication in BMDCs derived from IFNAR-deficient mice resulted in significantly more IL-1β release. Additionally, IL-1 receptor-deficient mice show an increase in RABV pathogenicity. Taken together, these results indicate an important role of the inflammasome in innate immune recognition of RABV.
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Registered trials
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.