ArticleThe Journal of biological chemistry2014
Transcriptional regulation of IFN-λ genes in hepatitis C virus-infected hepatocytes via IRF-3·IRF-7·NF-κB complex.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 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
28 citing papers in PubMed, 41 citations in OpenAlex.
- Interferon Regulatory Factors in Alcohol-Associated Liver Disease: Cell-Type Programs, Danger Signaling, and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- ATG10S promotes IFNL1 expression and autophagic degradation of multiple viral proteins mediated by IFNL1.Autophagy · 2024Article
- IntrahepaticViruses · 2021Article
- Functional genetic variants of the IFN-λ3 (IL28B) gene and transcription factor interactions on its promoter.Cytokine · 2021Article
- Liver Abnormalities after Elimination of HCV Infection: Persistent Epigenetic and Immunological Perturbations Post-Cure.Pathogens (Basel, Switzerland) · 2021Review
- A new transcription factor ATG10S activates IFNL2 transcription by binding at an IRF1 site in HepG2 cells.Autophagy · 2020Article
- The RNA binding protein Quaking represses host interferon response by downregulating MAVS.RNA biology · 2020Article
- Host immune response in chronic hepatitis C infection: involvement of cytokines and inflammasomes.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie · 2020Article
- Review
- Differential Effects of Autophagy-Related 10 Protein on HCV Replication and Autophagy Flux Are Mediated by Its CysteineFrontiers in immunology · 2018Article
- Long noncoding RNAs expression profile and functional networks in rheumatoid arthritis.Oncotarget · 2017Article
- Dual Roles of Two Isoforms of Autophagy-related Gene ATG10 in HCV-Subgenomic replicon Mediated Autophagy Flux and Innate Immunity.Scientific reports · 2017Article
- Contribution of type III interferons to antiviral immunity: location, location, location.The Journal of biological chemistry · 2017Review
- Hepatitis E virus persists in the presence of a type III interferon response.PLoS pathogens · 2017Article
- The Role of Type III Interferons in Hepatitis C Virus Infection and Therapy.Journal of immunology research · 2017Review
- The role of IL-29 in immunity and cancer.Critical reviews in oncology/hematology · 2016Review
- Dengue virus infection induces interferon-lambda1 to facilitate cell migration.Scientific reports · 2016Article
- Immune Activation in the Liver by Nucleic Acids.Journal of clinical and translational hepatology · 2016Review
- Mumps Virus Induces Protein-Kinase-R-Dependent Stress Granules, Partly Suppressing Type III Interferon Production.PloS one · 2016Article
- Immune and non-immune responses to hepatitis C virus infection.World journal of gastroenterology · 2015Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Hepatitis C virus (HCV) infection in hepatocytes stimulates innate antiviral responses including the production of type III interferons (IFN-λ), including IL-28A, IL-28B, and IL-29. However, the molecular mechanism(s) regulating the expression of IFN-λ genes in HCV-infected hepatocytes remains undefined. In this study, we examined regulatory elements involved in the induction of IFN-λ genes following HCV infection in hepatocytes and further determined the binding of specific transcription factor(s) to promoter regions of IFN-λ genes. Our studies reveal that the regulatory portion for IL-28A, IL-28B, and IL-29 genes is localized to a 1-kb region in their respective promoters. Notably, interferon regulatory factor (IRF)-3 and -7 are the key transcriptional factors for the induction of IL-28A and IL-28B genes, whereas NF-κB is an additional requirement for the induction of the IL-29 gene. Ligation of Toll-like receptors (TLR) 3, 7, 8, and 9, which also activate IRFs and NF-κB, resulted in more robust production of IFN-λ than that observed with HCV infection, verifying the importance of TLR pathways in IFN-λ production. Furthermore, the addition of IFN-λ to HCV-infected hepatocytes decreased viral replication and produced a concurrent reduction in microRNA-122 (miR-122). The decrease in viral replication was enhanced by the co-administration of IFN-λ and miR-122 inhibitor (miRIDIAN), suggesting that such combinatorial therapies may be beneficial for the treatment of chronic HCV infection.
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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.