ArticlePloS one2009
Toll-like receptor 3 signaling on macrophages is required for survival following coxsackievirus B4 infection.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 132 citations in OpenAlex.
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- Toll-like receptor 3: a double-edged sword.Biomarker research · 2025Review
- Immune repertoire profiling and T cell dysregulation in Peripheral Blood Mononuclear Cells of Type 2 diabetic patients.PloS one · 2025Article
- Genetic variation of TLR3 gene is associated with the outcome of hepatitis b infection in mauritanian patients: case control study.BMC infectious diseases · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Exosome-mediated delivery of gga-miR-20a-5p regulates immune response of chicken macrophages by targeting IFNGR2, MAPK1, MAP3K5, and MAP3K14.Animal bioscience · 2023Article
- Inborn errors of TLR3- or MDA5-dependent type I IFN immunity in children with enterovirus rhombencephalitis.The Journal of experimental medicine · 2021Article
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- Role of nucleic acid sensing in the pathogenesis of type 1 diabetes.World journal of diabetes · 2021Review
- Review
- Human cardiac fibroblasts produce pro-inflammatory cytokines upon TLRs and RLRs stimulation.Molecular and cellular biochemistry · 2021Article
- Cell type-specific roles of PAR1 in Coxsackievirus B3 infection.Scientific reports · 2021Article
- Review
- TLR3 controls constitutive IFN-β antiviral immunity in human fibroblasts and cortical neurons.The Journal of clinical investigation · 2021Article
- Virus in the pathogenesis of inflammatory bowel disease: role of Toll-like receptor 7/8/3.Gastroenterology and hepatology from bed to bench · 2021Review
- Changes in MDA5 and TLR3 Sensing of the Same Diabetogenic Virus Result in Different Autoimmune Disease Outcomes.Frontiers in immunology · 2021Article
- Immune Intervention in Sepsis.Frontiers in pharmacology · 2021Review
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- Enteroviruses and T1D: Is It the Virus, the Genes or Both which Cause T1D.Microorganisms · 2020Review
- Cell Surface Expression of Endosomal Toll-Like Receptors-A Necessity or a Superfluous Duplication?Frontiers in immunology · 2020Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 3 (TLR3) has been proposed to play a central role in the early recognition of viruses by sensing double stranded RNA, a common intermediate of viral replication. However, several reports have demonstrated that TLR3 signaling is either dispensable or even harmful following infection with certain viruses. Here, we asked whether TLR3 plays a role in the response to coxsackievirus B4 (CB4), a prevalent human pathogen that has been associated with pancreatitis, myocarditis and diabetes. We demonstrate that TLR3 signaling on macrophages is critical to establish protective immunity to CB4. TLR3 deficient mice produced reduced pro-inflammatory mediators and are unable to control viral replication at the early stages of infection resulting in severe cardiac damage. Intriguingly, the absence of TLR3 did not affect the activation of several key innate and adaptive cellular effectors. This suggests that in the absence of TLR3 signaling on macrophages, viral replication outpaces the developing adaptive immune response. We further demonstrate that the MyD88-dependent signaling pathways are not only unable to compensate for the loss of TLR3, they are also dispensable in the response to this RNA virus. Our results demonstrate that TLR3 is not simply part of a redundant system of viral recognition, but rather TLR3 plays an essential role in recognizing the molecular signatures associated with specific viruses including CB4.
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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.