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* Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021;
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; and
Department of Immunology, Institute for Cell Biology, University of Tübingen, Tübingen, Germany
The
-herpesvirus, EBV, is reliably found in a latent state in
endemic Burkitts lymphoma. A single EBV gene product, Epstein-Barr
nuclear Ag 1 (EBNA1), is expressed at the protein level. Several
mechanisms prevent immune recognition of these tumor cells, including a
block in EBNA1 presentation to CD8+ killer T cells.
Therefore, no EBV-specific immune response has yet been found to target
Burkitts lymphoma. We now find that EBNA1-specific, Th1
CD4+ cytotoxic T cells recognize Burkitts lymphoma lines.
CD4+ T cell epitopes of EBNA1 are predominantly found in
the C-terminal, episome-binding domain of EBNA1, and
0.5% of
peripheral blood CD4+ T cells are specific for EBNA1.
Therefore, adaptive immunity can be directed against Burkitts
lymphoma, and perhaps this role for CD4+ Th1 cells extends
to other tumors that escape MHC class I
presentation.
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