ArticleHepatology (Baltimore, Md.)2017
Central role of the TIR-domain-containing adaptor-inducing interferon-β (TRIF) adaptor protein in murine sterile liver injury.
Article in Hepatology (Baltimore, Md.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed, 12 citations in OpenAlex.
- TRIF-dependent signaling and its role in liver diseases.Frontiers in cell and developmental biology · 2024Review
- Response of Human Liver Tissue to Innate Immune Stimuli.Frontiers in immunology · 2022Article
- Methamphetamine-Induced Neuronal Damage: Neurotoxicity and Neuroinflammation.Biomolecules & therapeutics · 2020Review
- Precision-cut human liver slice cultures as an immunological platform.Journal of immunological methods · 2018Article
- TRIF as a Novel Modulator of Liver Inflammation and Fibrosis.Cellular and molecular gastroenterology and hepatology · 2017Article
- Toll-Like Receptor 4 Mediates Methamphetamine-Induced Neuroinflammation through Caspase-11 Signaling Pathway in Astrocytes.Frontiers in molecular neuroscience · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Multiple pathways drive the sterile injury response in the liver; however, it is unclear how the type of cells injured or the mechanism of injury activates these pathways. Here, we use a model of selective hepatocyte death to investigate sterile liver injury. In this model, the TIR-domain-containing adaptor-inducing interferon-β (TRIF) was a central mediator of the resulting intrahepatic inflammatory response that was independent of both upstream Toll-like receptor (TLR) 4 signaling and downstream type I interferon (IFN) signaling. TRIF was required for induction of interleukin (IL)-10, IL-6, and IL-1β cytokines. Conversely, although induction of C-C motif chemokine ligand (CCL) 2 and C-X-C motif chemokine ligand (CXCL) 1 chemokines and up-regulation of chemokine (Ccl2, Ccl7, Cxcl1, Cxcl2, and Cxcl10) and cell-adhesion (intracellular adhesion molecule 1 and vascular cell adhesion molecule 1) genes involved in myeloid cell recruitment was reduced in a majority of TRIF
conclusionOur studies define a TRIF-dependent, TLR4- and type I IFN-independent pathway of sterile liver injury in which hepatocytes are both the targets of damage and the principal responding cell type. (Hepatology 2017;65:1336-1351).
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