ArticleThe Journal of experimental medicine2004
CD8 T cell recognition of endogenously expressed epstein-barr virus nuclear antigen 1.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 154 citations in OpenAlex.
- Causal associations between antibody-mediated immune responses to infectious agents and cardiovascular inflammatory diseases: A Mendelian randomization study based on UK Biobank and FinnGen.Human vaccines & immunotherapeutics · 2026Article
- Molecular Mimicry Between Epstein-Barr Virus and Human Herpesvirus-6 Proteins and Central Nervous System Proteins: Implications for T and B Cell Immunogenicity in an In Silico Study.Immunity, inflammation and disease · 2026Article
- The Epstein-Barr virus EBNA1 protein binds to G-quadruplexes in its own mRNA hence controlling its expression and immune evasion of the virus.Nucleic acids research · 2025Article
- Mechanisms of T cell evasion by Epstein-Barr virus and implications for tumor survival.Frontiers in immunology · 2023Review
- EBV-induced T-cell responses in EBV-specific and nonspecific cancers.Frontiers in immunology · 2023Review
- Type I arginine methyltransferases are intervention points to unveil the oncogenic Epstein-Barr virus to the immune system.Nucleic acids research · 2022Article
- Article
- The Critical Role of Genome Maintenance Proteins in Immune Evasion During Gammaherpesvirus Latency.Frontiers in microbiology · 2018Review
- Macavirus latency-associated protein evades immune detection through regulation of protein synthesis in cis depending upon its glycin/glutamate-rich domain.PLoS pathogens · 2017Article
- Article
- Epstein-Barr Virus as a Promising Immunotherapeutic Target for Nasopharyngeal Carcinoma Treatment.Journal of pathogens · 2017Review
- Immunotherapy against cancer-related viruses.Cell research · 2017Review
- Article
- Elevation of c-MYC disrupts HLA class II-mediated immune recognition of human B cell tumors.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Adoptive T-Cell Immunotherapy.Current topics in microbiology and immunology · 2015Review
- Interference with the Autophagic Process as a Viral Strategy to Escape from the Immune Control: Lesson from Gamma Herpesviruses.Journal of immunology research · 2015Review
- mRNA Structural constraints on EBNA1 synthesis impact on in vivo antigen presentation and early priming of CD8+ T cells.PLoS pathogens · 2014Article
- A recombinant modified vaccinia ankara vaccine encoding Epstein-Barr Virus (EBV) target antigens: a phase I trial in UK patients with EBV-positive cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- G-quadruplexes regulate Epstein-Barr virus-encoded nuclear antigen 1 mRNA translation.Nature chemical biology · 2014Article
- Adenovirus-based vaccines against rhesus lymphocryptovirus EBNA-1 induce expansion of specific CD8+ and CD4+ T cells in persistently infected rhesus macaques.Journal of virology · 2014Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) nuclear antigen (EBNA)1 contains a glycine-alanine repeat (GAr) domain that appears to protect the antigen from proteasomal breakdown and, as measured in cytotoxicity assays, from major histocompatibility complex (MHC) class I-restricted presentation to CD8+ T cells. This led to the concept of EBNA1 as an immunologically silent protein that although unique in being expressed in all EBV malignancies, could not be exploited as a CD8 target. Here, using CD8+ T cell clones to native EBNA1 epitopes upstream and downstream of the GAr domain and assaying recognition by interferon gamma release, we show that the EBNA1 naturally expressed in EBV-transformed lymphoblastoid cell lines (LCLs) is in fact presented to CD8+ T cells via a proteasome/peptide transporter-dependent pathway. Furthermore, LCL recognition by such CD8+ T cells, although slightly lower than seen with paired lines expressing a GAr-deleted EBNA1 protein, leads to strong and specific inhibition of LCL outgrowth in vitro. Endogenously expressed EBNA1 is therefore accessible to the MHC class I pathway despite GAr-mediated stabilization of the mature protein. We infer that EBNA1-specific CD8+ T cells do play a role in control of EBV infection in vivo and might be exploitable in the control of EBV+ malignancies.
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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.