ArticleJournal of immunology (Baltimore, Md. : 1950)2010
In hepatic fibrosis, liver sinusoidal endothelial cells acquire enhanced immunogenicity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 116 citations in OpenAlex.
- Liver sinusoidal endothelial cells (LSECs) modifications in patients with chronic hepatitis C.Scientific reports · 2019Trial
- Liver sinusoidal endothelial cells constitute a major route for hemoglobin clearance.EMBO reports · 2026Article
- Antigen-specific tolerance and control of autoimmunity effected by liver sinusoidal endothelial cells is unimpaired in liver fibrosis.Frontiers in immunology · 2026Article
- Immune System and Hepatic Stellate Cells' Crosstalk in Liver Fibrosis: Pathways and Therapeutic Potential.Journal of immunology research · 2026Review
- Defenestration of Liver Sinusoidal Endothelial Cells: The Trigger of Liver Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Angiocrine signaling in sinusoidal homeostasis and liver diseases.Journal of hepatology · 2024Review
- Cellular uptake and in vivo distribution of mesenchymal-stem-cell-derived extracellular vesicles are protein corona dependent.Nature nanotechnology · 2024Article
- Liver sinusoidal endothelial cells as potential drivers of liver fibrosis (Review).Molecular medicine reports · 2024Article
- Functions and Clinical Relevance of Liver-Derived Immunoglobulins.Advances in experimental medicine and biology · 2024Review
- Targeting Endothelial Necroptosis Disrupts Profibrotic Endothelial-Hepatic Stellate Cells Crosstalk to Alleviate Liver Fibrosis in Nonalcoholic Steatohepatitis.International journal of molecular sciences · 2023Article
- RIPK3 promoter hypermethylation in hepatocytes protects from bile acid-induced inflammation and necroptosis.Cell death & disease · 2023Article
- Endotheliopathy in the metabolic syndrome: Mechanisms and clinical implications.Pharmacology & therapeutics · 2023Review
- Impact of immune tolerance mechanisms on the efficacy of immunotherapy in primary and secondary liver cancers.Translational gastroenterology and hepatology · 2023Review
- The immunological function of CXCR2 in the liver during sepsis.Journal of inflammation (London, England) · 2022Review
- The immunological mechanisms and therapeutic potential in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.Cell & bioscience · 2022Review
- Cancer cells produce liver metastasis via gap formation in sinusoidal endothelial cells through proinflammatory paracrine mechanisms.Science advances · 2022Article
- Review
- Harnessing the liver to induce antigen-specific immune tolerance.Seminars in immunopathology · 2022Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
The normal liver is characterized by immunologic tolerance. Primary mediators of hepatic immune tolerance are liver sinusoidal endothelial cells (LSECs). LSECs block adaptive immunogenic responses to Ag and induce the generation of T regulatory cells. Hepatic fibrosis is characterized by both intense intrahepatic inflammation and altered hepatic immunity. We postulated that, in liver fibrosis, a reversal of LSEC function from tolerogenic to proinflammatory and immunogenic may contribute to both the heightened inflammatory milieu and altered intrahepatic immunity. We found that, after fibrotic liver injury from hepatotoxins, LSECs become highly proinflammatory and secrete an array of cytokines and chemokines. In addition, LSECs gain enhanced capacity to capture Ag and induce T cell proliferation. Similarly, unlike LSECs in normal livers, in fibrosis, LSECs do not veto dendritic cell priming of T cells. Furthermore, whereas in normal livers, LSECs are active in the generation of T regulatory cells, in hepatic fibrosis LSECs induce an immunogenic T cell phenotype capable of enhancing endogenous CTLs and generating potent de novo CTL responses. Moreover, depletion of LSECs from fibrotic liver cultures mitigates the proinflammatory milieu characteristic of hepatic fibrosis. Our findings offer a critical understanding of the role of LSECs in modulating intrahepatic immunity and inflammation in fibro-inflammatory liver disease.
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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.