ArticlePloS one2014
Quiescent hepatic stellate cells functionally contribute to the hepatic innate immune response via TLR3.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- AURKA regulates HBV-induced hepatic stellate cell inflammation and liver fibrosis by modulating K48-linked ubiquitination and proteasomal degradation of TLR3.Journal of bioenergetics and biomembranes · 2026Article
- Epigenetic drug control of Clec4g/LSECtin expression reduces fibrosis burden in cirrhosis.Hepatology communications · 2026Article
- Pharmacological manipulation of liver fibrosis progression using novel HDAC6 inhibitors.The FEBS journal · 2025Article
- The mechanism of p38 MAPK, NF-κB, and IL-6 in T-2 toxin and/or selenium deficiency induced spleen injury.Immunologic research · 2025Article
- Interorgan communication with the liver: novel mechanisms and therapeutic targets.Frontiers in immunology · 2023Review
- Hepatic Stellate Cell-Immune Interactions in NASH.Frontiers in endocrinology · 2022Review
- Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis-Roles as Putative Treatment Targets?Biomedicines · 2021Review
- The cellular pathways of liver fibrosis in non-alcoholic steatohepatitis.Annals of translational medicine · 2020Review
- Embryonic mesothelial-derived hepatic lineage of quiescent and heterogenous scar-orchestrating cells defined but suppressed by WT1.Nature communications · 2019Article
- Fibroblasts Promote Inflammation and Pain via IL-1α Induction of the Monocyte Chemoattractant Chemokine (C-C Motif) Ligand 2.The American journal of pathology · 2018Article
- TLR3 Activation of Hepatic Stellate Cell Line Suppresses HBV Replication in HepG2 Cells.Frontiers in immunology · 2018Article
- Magnesium Isoglycyrrhizinate Ameliorates Fibrosis and Disrupts TGF-β-Mediated SMAD Pathway in Activated Hepatic Stellate Cell Line LX2.Frontiers in pharmacology · 2018Article
- Vascular endothelial growth factor promotes the activation of hepatic stellate cells in chronic schistosomiasis.Immunology and cell biology · 2017Article
- Association of Toll-Like Receptor 3 Single-Nucleotide Polymorphisms and Hepatitis C Virus Infection.Journal of immunology research · 2017Article
- Intrahepatic regulation of antiviral T cell responses at initial stages of viral infection.International immunopharmacology · 2016Review
- Selenoproteins and heat shock proteins play important roles in immunosuppression in the bursa of Fabricius of chickens with selenium deficiency.Cell stress & chaperones · 2015Article
- Cellular and molecular functions of hepatic stellate cells in inflammatory responses and liver immunology.Hepatobiliary surgery and nutrition · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Toll-like Receptor 3 (TLR3) is a pathogen pattern recognition receptor that plays a key role in innate immunity. TLR3 signalling has numerous functions in liver, both in health and disease. Here we report that TLR3 is expressed by quiescent hepatic stellate cells (HSC) where it functions to induce transcription and secretion of functional interferons as well as a number of other cytokines and chemokines. Upon transdifferentiation into myofibroblasts, HSCs rapidly loose the ability to produce interferon gamma (IFNγ). Mechanistically, this gene silencing may be due to Polycomb complex mediated repression via methylation of histone H3 lysine 27. In contrast to wild type, quiescent HSC isolated from tlr3 knockout mice do not produce IFNγ in response to Poly(I∶C) treatment. Therefore, quiescent HSC may contribute to induction of the hepatic innate immune system in response to injury or infection.
Indexed as
Identifiers
What OpenQuestion holds
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.