ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Inflammatory regulation by TLR3 in acute hepatitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Recent advances in different interactions between toll-like receptors and hepatitis B infection: a review.Frontiers in immunology · 2024Review
- TLR3 Gene Polymorphism in HCV Infection in the Kazakh Population of Western Kazakhstan.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- LIGHT Amplification by NF-Mediators of inflammation · 2023Article
- Article
- Integrated intra- and intercellular signaling knowledge for multicellular omics analysis.Molecular systems biology · 2021Article
- Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020Review
- Central role of the TIR-domain-containing adaptor-inducing interferon-β (TRIF) adaptor protein in murine sterile liver injury.Hepatology (Baltimore, Md.) · 2017Article
- Association of Toll-Like Receptor 3 and Toll-Like Receptor 9 Single Nucleotide Polymorphisms with Hepatitis C Virus Infection and Hepatic Fibrosis in Egyptian Patients.The American journal of tropical medicine and hygiene · 2017Article
- Chronic Inflammation in Immune Aging: Role of Pattern Recognition Receptor Crosstalk with the Telomere Complex?Frontiers in immunology · 2017Review
- Mincle Signaling Promotes Con A Hepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Increased expression of endosomal members of toll-like receptor family abrogates wound healing in patients with type 2 diabetes mellitus.International wound journal · 2016Article
- Interferon β (IFN-β) Production during the Double-stranded RNA (dsRNA) Response in Hepatocytes Involves Coordinated and Feedforward Signaling through Toll-like Receptor 3 (TLR3), RNA-dependent Protein Kinase (PKR), Inducible Nitric Oxide Synthase (iNOS), and Src Protein.The Journal of biological chemistry · 2016Article
- Quercetin Protects Mice from ConA-Induced Hepatitis by Inhibiting HMGB1-TLR Expression and Down-Regulating the Nuclear Factor Kappa B Pathway.Inflammation · 2016Article
- Role of toll-like receptors in immune activation and tolerance in the liver.Frontiers in immunology · 2014Review
- The role of vitamin d in autoimmune hepatitis.Journal of clinical medicine research · 2013Review
- The great escape: microbiotal LPS takes a toll on the liver.Cancer prevention research (Philadelphia, Pa.) · 2012Article
- The roles of Galectin-3 in autoimmunity and tumor progression.Immunologic research · 2012Review
- IL-33/ST2 axis in inflammation and immunopathology.Immunologic research · 2012Review
- Toll-like receptor 3 in liver diseases.Gastroenterology research and practice · 2010Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 5 countries.
Funding
Abstract
TLR3 is known to respond to dsRNA from viruses, apoptotic cells, and/or necrotic cells. Dying cells are a rich source of ligands that can activate TLRs, such as TLR3. TLR3 expressed in the liver is likely to be a mediator of innate activation and inflammation in the liver. The importance of this function of TLR3 during acute hepatitis has not previously been fully explored. We used the mouse model of Con A-induced hepatitis and observed a novel role for TLR3 in hepatocyte damage in the absence of an exogenous viral stimulus. Interestingly, TLR3 expression in liver mononuclear cells and sinus endothelial cells was up-regulated after Con A injection and TLR3(-/-) mice were protected from Con A-induced hepatitis. Moreover, splenocytes from TLR3(-/-) mice proliferated less to Con A stimulation in the presence of RNA derived from damaged liver tissue compared with wild-type (WT) mice. To determine the relative contribution of TLR3 expression by hematopoietic cells or nonhematopoietic to liver damage during Con A-induced hepatitis, we generated bone marrow chimeric mice. TLR3(-/-) mice engrafted with WT hematopoietic cells were protected in a similar manner to WT mice reconstituted with TLR3(-/-) bone marrow, indicating that TLR3 signaling in both nonhematopoietic and hematopoietic cells plays an important role in mediating liver damage. In summary, our data suggest that TLR3 signaling is necessary for Con A-induced liver damage in vivo and that TLR3 regulates inflammation and the adaptive T cell immune response in the absence of viral infection.
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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.