ArticlePLoS pathogens2006
Detrimental contribution of the Toll-like receptor (TLR)3 to influenza A virus-induced acute pneumonia.
Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 288 papers.
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Who cites it
288 citing papers in PubMed, 503 citations in OpenAlex.
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- Combined network pharmacology and biological verification to investigate anti-influenza A virus effect and potential mechanism of Pudilan Xiaoyan Oral Liquid.Chinese herbal medicines · 2026Article
- Update on the Efficacy of Vaccination on Host Immunity to Influenza Virus Infection.International archives of allergy and immunology · 2026Review
- Cis-aconitate therapy protects against influenza mortality by dual targeting of viral polymerase and ERK/AKT/NF-κB signaling.EMBO molecular medicine · 2026Article
- Macrophage makeover extreme viral edition: mechanisms of immune subversion and therapeutic perspectives.The Journal of general virology · 2026Review
- Review
- Polyinosinic Polycytidylic Acid (poly I:C) Induces Neuronal Cell Death Through NF-κB-Mediated Inflammation in Human Microglia and Neuroinflammation-Induced Cognitive Impairment in Mice.Molecular neurobiology · 2025Article
- Plasmacytoid dendritic cells are dispensable or detrimental in murine systemic or respiratory viral infections.Nature immunology · 2025Article
- Molecular characterization of endosomal self RNA Rmrp-engaged TLR3 dimerization to prime innate activation.Cell research · 2025Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- lncRNALife science alliance · 2025Article
- Toll-like receptor 3: a double-edged sword.Biomarker research · 2025Review
- Innate Sensing of Viral Nucleic Acids and Their Use in Antiviral Vaccine Development.Vaccines · 2025Review
- IFN-γ primes bone marrow neutrophils to acquire regulatory functions in severe viral respiratory infections.Science advances · 2024Article
- The deadly dance of alveolar macrophages and influenza virus.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Defining the balance between optimal immunity and immunopathology in influenza virus infection.Nature reviews. Immunology · 2024Review
- Host Innate Antiviral Response to Influenza A Virus Infection: From Viral Sensing to Antagonism and Escape.Pathogens (Basel, Switzerland) · 2024Review
- Recent Insights into the Molecular Mechanisms of the Toll-like Receptor Response to Influenza Virus Infection.International journal of molecular sciences · 2024Review
- TRIF-dependent signaling and its role in liver diseases.Frontiers in cell and developmental biology · 2024Review
- Sodium-Glucose Cotransporter-2 Inhibitor, Empagliflozin, Suppresses the Inflammatory Immune Response to Influenza Infection.ImmunoHorizons · 2023Article
228 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) is the etiological agent of a highly contagious acute respiratory disease that causes epidemics and considerable mortality annually. Recently, we demonstrated, using an in vitro approach, that the pattern recognition Toll-like receptor (TLR)3 plays a key role in the immune response of lung epithelial cells to IAV. In view of these data and the fact that the functional role of TLR3 in vivo is still debated, we designed an investigation to better understand the role of TLR3 in the mechanisms of IAV pathogenesis and host immune response using an experimental murine model. The time-course of several dynamic parameters, including animal survival, respiratory suffering, viral clearance, leukocyte recruitment into the airspaces and secretion of critical inflammatory mediators, was compared in infected wild-type and TLR3(-/-) mice. First, we found that the pulmonary expression of TLR3 is constitutive and markedly upregulated following influenza infection in control mice. Notably, when compared to wild-type mice, infected TLR3-/- animals displayed significantly reduced inflammatory mediators, including RANTES (regulated upon activation, normal T cell expressed and secreted), interleukin-6, and interleukin-12p40/p70 as well as a lower number of CD8+ T lymphocytes in the bronchoalveolar airspace. More important, despite a higher viral production in the lungs, mice deficient in TLR3 had an unexpected survival advantage. Hence, to our knowledge, our findings show for the first time that TLR3-IAV interaction critically contributes to the debilitating effects of a detrimental host inflammatory response.
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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.