ArticleJournal of immunology (Baltimore, Md. : 1950)2012
A TRIF-independent branch of TLR3 signaling.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Toll-like Receptor 3 as a Context-Dependent Molecular Switch in Epithelial Cancers: Balancing Cell Death and Tumor-Supportive Programs.International journal of molecular sciences · 2026Review
- Rewiring of host cell signaling in chikungunya virus infection: a mechanism for pathogenesis and therapeutic approaches.Archives of microbiology · 2026Review
- Immune and Stem Cell Interactions in Periodontal Disease: The Regulatory Role of Toll-Like Receptor 3.Advances in experimental medicine and biology · 2026Review
- Article
- Regulation of interferon alpha production by the MAGUK-family protein CASK under H5N1 infection.Frontiers in immunology · 2024Article
- EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Unexpected Need of the Epidermal Growth Factor Receptor Tyrosine Kinase Activity for Signaling by Intracellular Pattern Recognition Receptors of Nucleic Acids.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Review
- TLR3-Activated Monocyte-Derived Dendritic Cells Trigger Progression from Acute Viral Infection to Chronic Disease in the Lung.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Human Innate Lymphoid Cells in Influenza Infection and Vaccination.Critical reviews in immunology · 2021Review
- RNA Signaling in Pulmonary Arterial Hypertension-A Double-Stranded Sword.International journal of molecular sciences · 2020Review
- When Innate Immunity Meets Angiogenesis-The Role of Toll-Like Receptors in Endothelial Cells and Pulmonary Hypertension.Frontiers in medicine · 2020Review
- Quantification of Infectious Sendai Virus Using Plaque Assay.Bio-protocol · 2018Article
- Sendai Virus Propagation Using Chicken Eggs.Bio-protocol · 2018Article
- Dengue virus infection increases microglial cell migration.Scientific reports · 2017Article
- Toll-like receptor 3 regulates NK cell responses to cytokines and controls experimental metastasis.Oncoimmunology · 2015Article
- Tyrosine phosphorylation in Toll-like receptor signaling.Cytokine & growth factor reviews · 2014Review
- dsRNA-activation of TLR3 and RLR signaling: gene induction-dependent and independent effects.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Flotillin-1 facilitates toll-like receptor 3 signaling in human endothelial cells.Basic research in cardiology · 2014Article
- GATA-3 regulates the self-renewal of long-term hematopoietic stem cells.Nature immunology · 2013Article
- Toll-like receptor 3 in viral pathogenesis: friend or foe?Immunology · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
dsRNA is a common pathogen-associated molecular pattern that is recognized by cellular TLR3 and used by virus-infected cells to activate specific transcription factors and trigger induction of antiviral genes. In this article, we report a new branch of TLR3 signaling that does not lead to gene induction but affects many cellular properties, such as cell migration, adhesion, and proliferation. We demonstrated that the migration of multiple cell lineages was affected by dsRNA treatment or influenza virus infection in a TLR3-dependent fashion. Surprisingly, for this effect of TLR3 signaling, the adaptor proteins, TRIF and MyD88, were not required. The effects of the new pathway were mediated by the proto-oncoprotein c-Src, which bound to TLR3 after dsRNA stimulation of cells. The response was biphasic: upon dsRNA treatment, we observed an immediate increase in cell motility followed by its strong inhibition. Our results indicate that the first phase was mediated by dsRNA-induced phosphorylation and activation of Src, whereas the second phase resulted from the sequestration of activated Src in lipid rafts, thus decreasing its active cytoplasmic pool. As expected, two other functions of Src, its effect on cell adhesion and cell proliferation, were also inhibited by dsRNA treatment. These results demonstrate that activated TLR3 can engage Src to trigger multiple cellular effects and reveal a possible link between innate immune response and cell growth regulation. This study also provides a rare example of TLR-mediated cellular effects that do not require gene induction and the first example, to our knowledge, of an adaptor-independent effect of any TLR.
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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.