HUMAN CYTOTOXIC T LYMPHOCYTE RESPONSES TO EPSTEIN-BARR VIRUS INFECTION

Article Properties
  • Language
    English
  • Publication Date
    1997/04/01
  • Indian UGC (Journal)
  • Refrences
    135
  • Citations
    548
  • Alan B. Rickinson CRC Institute for Cancer Studies, University of Birmingham, Birmingham, B15 2TT, United Kingdom;
  • Denis J. Moss Queensland Institute of Medical Research, Bramston Terrace, Herston, Brisbane 4006, Australia
Abstract
Cite
Rickinson, Alan B., and Denis J. Moss. “HUMAN CYTOTOXIC T LYMPHOCYTE RESPONSES TO EPSTEIN-BARR VIRUS INFECTION”. Annual Review of Immunology, vol. 15, no. 1, 1997, pp. 405-31, https://doi.org/10.1146/annurev.immunol.15.1.405.
Rickinson, A. B., & Moss, D. J. (1997). HUMAN CYTOTOXIC T LYMPHOCYTE RESPONSES TO EPSTEIN-BARR VIRUS INFECTION. Annual Review of Immunology, 15(1), 405-431. https://doi.org/10.1146/annurev.immunol.15.1.405
Rickinson AB, Moss DJ. HUMAN CYTOTOXIC T LYMPHOCYTE RESPONSES TO EPSTEIN-BARR VIRUS INFECTION. Annual Review of Immunology. 1997;15(1):405-31.
Journal Categories
Medicine
Internal medicine
Specialties of internal medicine
Immunologic diseases
Allergy
Description

What drives the human immune system's fight against Epstein-Barr virus? This review dives into cytotoxic T lymphocyte (CTL) responses in humans, using Epstein-Barr virus (EBV) as a highly informative model. EBV establishes a highly immunogenic growth-transforming infection of B lymphocytes, inducing the expression of six virus-coded nuclear antigens (EBNAs) and two latent membrane proteins (LMPs). This triggers both primary and memory CD8+ CTL responses, skewed towards HLA allele-specific epitopes drawn from the EBNA3A, 3B, 3C subset of latent proteins. Other antigens elicit far less frequent responses. Furthermore, CTLS to some of the immunodominant epitopes may cause TCR usage, which suggest could have immunopathological consequences from cross-reactive recognition of other target structures. Targeting EBV-associated tumors, dramatic reversals of EBV-driven lymphoproliferations have been observed in transplant patients following CTL infusion. The review explores the potential of this approach for other EBV-positive tumors lacking EBNA3A, 3B, 3C proteins. It offers insights into EBV-associated malignancies and CTL-based therapeutic strategies.

Published in Annual Review of Immunology, this paper clearly fits the journal's mission by providing a comprehensive overview of CTL responses to EBV infection, a major topic in human immunology. The review's focus on the EBNA3A, 3B, and 3C proteins, their immunodominance, and potential therapeutic applications is of significant interest to the journal's readership.

Refrences
Citations
Citations Analysis
The first research to cite this article was titled Epstein–Barr virus-induced gene 3 and the p35 subunit of interleukin 12 form a novel heterodimeric hematopoietin and was published in 1997. The most recent citation comes from a 2024 study titled Epstein–Barr virus-induced gene 3 and the p35 subunit of interleukin 12 form a novel heterodimeric hematopoietin . This article reached its peak citation in 2002 , with 52 citations.It has been cited in 197 different journals, 16% of which are open access. Among related journals, the Blood Journal cited this research the most, with 47 citations. The chart below illustrates the annual citation trends for this article.
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