The Journal of Experimental Medicine
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Published 1 December 2003. doi:10.1084/jem.20030646
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© Rockefeller University Press, 0022-1007/2003/12/1653 $5.00
The Journal of Experimental Medicine, Volume 198, Number 11, 1653-1663

Dendritic Cells Initiate Immune Control of Epstein-Barr Virus Transformation of B Lymphocytes In Vitro

Kara Bickham1,2, Kiera Goodman1,2, Casper Paludan1,2, Sarah Nikiforow3, Ming Li Tsang1,2, Ralph M. Steinman1,2 and Christian Münz1,2

1 Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021
2 The Chris Browne Center for Immunology and Immune Disease, The Rockefeller University, New York, NY 10021
3 Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520

Address correspondence to Christian Münz, Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021. Phone: (212) 327-7611; Fax: (212) 327-7887; email: munzc{at}mail.rockefeller.edu

The initiation of cell-mediated immunity to Epstein-Barr virus (EBV) has been analyzed with cells from EBV-seronegative blood donors in culture. The addition of dendritic cells (DCs) is essential to prime naive T cells that recognize EBV-latent antigens in enzyme-linked immunospot assays for interferon {gamma} secretion and eradicate transformed B cells in regression assays. In contrast, DCs are not required to control the outgrowth of EBV-transformed B lymphocytes from seropositive donors. Enriched CD4+ and CD8+ T cells mediate regression of EBV-transformed cells in seronegative and seropositive donors, but the kinetics of T-dependent regression occurs with much greater speed with seropositives. EBV infection of DCs cannot be detected by reverse transcription–polymerase chain reaction with primers specific for mRNA for the EBNA1 U and K exons. Instead, DCs capture B cell debris and generate T cells specific for EBV latency antigens. We suggest that the cross-presentation of EBV-latent antigens from infected B cells by DCs is required for the initiation of EBV-specific immune control in vivo and that future EBV vaccine strategies should target viral antigens to DCs.

Key Words: herpesvirus • regression assay • cross-priming • T cell • B cell

The online version of this article includes supplemental material.

Abbreviations used in this paper: CSA, cyclosporin A; EBV, Epstein-Barr virus; HD, Hodgkin's disease; IM, infectious mononucleosis; LCL, lymphoblastoid cell line; PTLD, posttransplant lymphoproliferative disease; vv, vaccinia viruses.


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