The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/2/445/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 3, February 2, 1998 445-450

Brief Definitive Reports

Murine Cytotoxic T Lymphocytes Recognize an Epitope in an EBNA-1 Fragment, but Fail to Lyse EBNA-1–expressing Mouse Cells

Siddhartha Mukherjee*, Pankaj Trivedi||, David M. Dorfman§, George Klein{ddagger}, and Alain Townsend*

From the * Molecular Immunology Group, Institute for Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, OX39DU, United Kingdom; {ddagger} Microbiology and Tumor Biology Center (MTC), Karolinska Institute, 171 77, Stockholm, Sweden; § Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts; and || INM, Neuromed, Localita Camerelle, 86077, Pozzilli (IS), Italy

Major histocompatibility complex class I–restricted cytotoxic T lymphocytes (CTLs) specific for epitopes within eight of the nine Epstein Barr Virus (EBV)-encoded latency-associated proteins have been recovered from EBV-infected human subjects by restimulation of lymphocytes in vitro. However, human class I–restricted CTL responses capable of recognizing EBNA-1 expressing cells were not detected in these studies. We have raised a murine CTL line that recognizes an epitope within EBNA-1 by immunizing mice with a vaccinia virus encoding a COOH-terminal EBNA-1 fragment. This novel CTL line was used to investigate whether the epitope (positions 509–517 in EBNA-1, presented through Kd) was presented to CTL by mouse cells expressing full-length EBNA-1 or a deletion mutant of EBNA-1, lacking the Glycine-Alanine (Gly-Ala)–rich region. Cells expressing full-length EBNA-1 are not lysed by the CTL line, whereas cells expressing the Gly-Ala deletion mutant are recognized. These results suggest that epitopes from full-length EBNA-1 are poorly presented, and that the Gly-Ala–rich region is responsible for this phenomenon. The inefficient presentation of EBNA-1–derived epitopes may explain the absence or rarity of EBNA-1–specific CTLs in vivo, a strategy that may allow EBV to maintain persistence within the immunocompetent host without being eliminated by CTLs.

Address correspondence to Siddhartha Mukherjee, Molecular Immunology Group, Institute for Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, OX39DU, UK.

S. Mukherjee was supported by the Rhodes Trust. P. Trivedi was supported by a grant from the Istituto Superiore di Sanita, Italy.


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