ArticlePloS one2007
Protection of hepatocytes from cytotoxic T cell mediated killing by interferon-alpha.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Human hepatic cell line 5: In-vitro model for hepatic immunobiology.Molecular biology reports · 2026Article
- Multiomics Analysis Reveals the Impact of Microbiota on Host Metabolism in Hepatic Steatosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Modelling Nonalcoholic Steatohepatitis In Vivo-A Close Transcriptomic Similarity Supports the Guinea Pig Disease Model.Biomedicines · 2021Article
- Evaluation of a range of mammalian and mosquito cell lines for use in Chikungunya virus research.Scientific reports · 2017Article
- Reduced circulating levels of sTWEAK are associated with NAFLD and may affect hepatocyte triglyceride accumulation.International journal of obesity (2005) · 2016Observational
- Mechanism of Hepatocyte Apoptosis.Journal of cell death · 2016Review
- [Efficacy of combination antiviral therapy following childbirth in pregnant HBV carriers receiving telbivudine for prevention of mother-to-child transmission].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2015Article
- MAIT cells are licensed through granzyme exchange to kill bacterially sensitized targets.Mucosal immunology · 2015Article
- Immortalized Human Hepatic Cell Lines for In Vitro Testing and Research Purposes.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Immune response of cytotoxic T lymphocytes and possibility of vaccine development for hepatitis C virus infection.Journal of biomedicine & biotechnology · 2010Article
- Treatment failure in hepatitis C: mechanisms of non-response.Journal of hepatology · 2009Review
- Natural killer cells in immunodefense against infective agents.Expert review of anti-infective therapy · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundCellular immunity plays a key role in determining the outcome of hepatitis C virus (HCV) infection, although the majority of infections become persistent. The mechanisms behind persistence are still not clear; however, the primary site of infection, the liver, may be critical. We investigated the ability of CD8+ T-cells (CTL) to recognise and kill hepatocytes under cytokine stimulation. METHODS/PRINCIPLE
findingsResting hepatocytes cell lines expressed low levels of MHC Class I, but remained susceptible to CTL cytotoxicity. IFN-alpha treatment, in vitro, markedly increased hepatocyte MHC Class I expression, however, reduced sensitivity to CTL cytotoxicity. IFN-alpha stimulated hepatocyte lines were still able to present antigen and induce IFN-gamma expression in interacting CTL. Resistance to killing was not due to the inhibition of the FASL/FAS- pathway, as stimulated hepatocytes were still susceptible to FAS-mediated apoptosis. In vitro stimulation with IFN-alpha, or the introduction of a subgenomic HCV replicon into the HepG2 line, upregulated the expression of the granzyme-B inhibitor-proteinase inhibitor 9 (PI-9). PI-9 expression was also observed in liver tissue biopsies from patients with chronic HCV infection. CONCLUSION/SIGNIFICANCE: IFN-alpha induces resistance in hepatocytes to perforin/granzyme mediate CTL killing pathways. One possible mechanism could be through the expression of the PI-9. Hindrance of CTL cytotoxicity could contribute to the chronicity of hepatic viral infections.
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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.