ArticleThe American journal of pathology2005
The HLA-A2 restricted T cell epitope HCV core 35-44 stabilizes HLA-E expression and inhibits cytolysis mediated by natural killer cells.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 171 citations in OpenAlex.
- Hepatitis C Virus Sensing by Human Trophoblasts Induces Innate Immune Responses and Recruitment of Maternal NK Cells: Potential Implications for Limiting Vertical Transmission.Journal of immunology (Baltimore, Md. : 1950) · 2015Trial
- Natural killer cells against viral infection: from basic biology to immunotherapy.Precision clinical medicine · 2026Review
- HLA-E-Directed Accumulation of KIRInternational journal of molecular sciences · 2026Article
- HLA class I signal peptide variation predicts strength of NKG2ANature immunology · 2026Article
- Shared HLA-E and Mamu-E Peptide Repertoires With Subtle Peptide Binding Differences Revealed by Combined nDSF- and Fluorescence Polarisation-Based Methods.European journal of immunology · 2026Article
- T cell dysfunction and metabolic disruption in chronic hepatitis C virus infection.Frontiers in immunology · 2026Review
- Hantaan virus-derived peptides that stabilize HLA-E could abrogate inhibition of CD56dimNKG2A+ NK cells.PLoS pathogens · 2025Article
- Elephant in the room: natural killer cells don't forget HIV either.Current opinion in HIV and AIDS · 2025Review
- HLA-E: Immune Receptor Functional Mechanisms Revealed by Structural Studies.Immunological reviews · 2025Review
- Viral sequence determines HLA-E-restricted T cell recognition of hepatitis B surface antigen.Nature communications · 2024Article
- Polygenic polymorphism is associated with NKG2A repertoire and influences lymphocyte phenotype and function.Blood advances · 2024Article
- Implications of NKG2A in immunity and immune-mediated diseases.Frontiers in immunology · 2022Review
- The Loss of HLA-F/KIR3DS1 Ligation Is Mediated by Hemoglobin Peptides.International journal of molecular sciences · 2020Article
- Control of HCV Infection by Natural Killer Cells and Macrophages.Cold Spring Harbor perspectives in medicine · 2020Review
- Immunomodulation of the Natural Killer Cell Phenotype and Response during HCV Infection.Journal of clinical medicine · 2020Review
- What the HLA-I!-Classical and Non-classical HLA Class I and Their Potential Roles in Type 1 Diabetes.Current diabetes reports · 2019Review
- Dimorphism of HLA-E and its Disease Association.International journal of molecular sciences · 2019Review
- Review
- Hepatitis C Virus Infection: Host⁻Virus Interaction and Mechanisms of Viral Persistence.Cells · 2019Review
- NKG2A is a NK cell exhaustion checkpoint for HCV persistence.Nature communications · 2019Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired activity of natural killer cells has been proposed as a mechanism contributing to viral persistence in hepatitis C virus (HCV) infection. Natural cytotoxicity is regulated by interactions of HLA-E with inhibitory CD94/NKG2A receptors on natural killer (NK) cells. Here, we studied whether HCV core encodes peptides that bind to HLA-E and inhibit natural cytotoxicity. We analyzed 30 HCV core-derived peptides. Peptide-induced stabilization of HLA-E expression was measured flow cytometrically after incubating HLA-E-transfected cells with peptides. NK cell function was studied with a (51)chromium-release-assay. Intrahepatic HLA-E expression was analyzed by an indirect immunoperoxidase technique and flow cytometry of isolated cells using a HLA-E-specific antibody. We identified peptide aa35-44, a well-characterized HLA-A2 restricted T cell epitope, as a peptide stabilizing HLA-E expression and thereby inhibiting NK cell-mediated lysis. Blocking experiments confirmed that this inhibitory effect of peptide aa35-44 on natural cytotoxicity was mediated via interactions between CD94/NKG2A receptors and enhanced HLA-E expression. In line with these in vitro data we found enhanced intrahepatic HLA-E expression on antigen-presenting cells in HCV-infected patients. Our data indicate the existence of T cell epitopes that can be recognized by HLA-A2 and HLA-E. This dual recognition may contribute to viral persistence in hepatitis C.
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