ArticleClinical and experimental medicine2020
Direct-acting antiviral treatment downregulates immune checkpoint inhibitor expression in patients with chronic hepatitis C.
Article in Clinical and experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Cure of chronic hepatitis C virus infection after DAA treatment only partially restores the functional capacity of exhausted T cell subsets: a systematic review.Frontiers in immunology · 2025Pooled it
- Diabetes Mellitus Increases the Risk of Hepatocellular Carcinoma After Direct-Acting Antiviral Therapy: Systematic Review and Meta-Analysis.Frontiers in medicine · 2021Pooled it
- Hepatitis C virus and extrahepatic malignancies: where we stand and how we can advance the field.Translational cancer research · 2026Article
- Hepatitis C in the Direct-Acting Antiviral Era: Immunopathogenesis, Dendritic Cells and Modern Clinical Management.Biomedicines · 2026Review
- Role of soluble human leukocyte antigen-G in virus-associated cancers: A focused minireview.World journal of virology · 2026Review
- T cell dysfunction and metabolic disruption in chronic hepatitis C virus infection.Frontiers in immunology · 2026Review
- Precision Strategy for Hepatocellular Carcinoma Surveillance after Hepatitis C Cure: Debates across Guidelines.Gut and liver · 2025Review
- Unveiling the nexus between direct-acting antivirals in hepatitis C virus elimination and immune response.Clinical and experimental medicine · 2025Review
- Natural killer cells in liver transplantation: Can we harness the power of the immune checkpoint to promote tolerance?Clinical and translational science · 2022Review
- Cancer in People with and without Hepatitis C Virus Infection: Comparison of Risk Before and After Introduction of Direct-Acting Antivirals.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021Observational
- Linking peripheral CD8Clinical and translational medicine · 2021Article
- HCV Cure With Direct-Acting Antivirals Improves Liver and Immunological Markers in HIV/HCV-Coinfected Patients.Frontiers in immunology · 2021Article
- Lymphocyte Landscape after ChronicInternational journal of molecular sciences · 2020Review
- Different Expression Pattern of TIM-3 and Galectin-9 Molecules by Peripheral and Peritoneal Lymphocytes in Women with and without Endometriosis.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Chronic hepatitis C (CHC) infection is associated with increased TIM-3, PD-1 immune checkpoint receptors expression that inhibits adaptive T cells and increases NK cell cytotoxicity against T helper cells, both resulting T cell exhaustion. Elimination of the virus with direct-acting antivirals (DAAs) may modify host immune response via altering these immune checkpoint receptors' expression. We conducted a prospective study to analyze changes in TIM-3, PD-1 and their ligands galectin-9, PD-L1 expression by peripheral blood T cell subpopulations, NK cell subpopulations, and monocytes by multicolor flow cytometry in 14 CHC patients successfully treated with 12 weeks of dasabuvir, ombitasvir, and paritaprevir/ritonavir plus ribavirin. Blood samples were collected before, at the end of treatment, and 12 and 24 weeks later. Sustained virological response (SVR) was associated with increased percentage of peripheral blood CD3+ T and CD8+ cytotoxic T lymphocytes and decreased percentage of NKbright cells. After DAA treatment, decreased TIM-3 expression by CD4+ T cells, by NKbright, and by NKT cells was found. Expression of immune checkpoint molecules' ligand PD-L1 by NK cells and by regulatory T cells and galectin-9 by NK cells and monocytes also decreased significantly at SVR. Our data suggest that DAA treatment not only inhibits viral replication but may alter host adaptive and innate immune responses. A decrease in immune checkpoint molecules and their ligands expression both on adaptive and on innate immune cells may contribute to the recovery of exhausted adaptive immune responses and to sustained virological response.
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