Abstract
The pathogenesis of Epstein–Barr (EB) virus-positive Burkitt's lymphoma (BL) appears to involve the combined actions of (1) virus-induced B-cell proliferation, and (2) a rare chromosomal translocation juxtaposing c-myc and immunoglobulin gene loci in a single B cell; holoendemic malarial infection in some way facilitates the oncogenic process1–3. Outgrowth of the EB virus-positive tumour suggests either breakdown or evasion of those immune controls, in particular cytotoxic T-cell responses against the virus-induced lymphocyte-detected membrane antigen LYDMA, which limit virus-infected B-cell numbers in healthy virus carriers4. Immunosuppression, such as that which malarial infection may induce5,6, cannot itself be a sufficient explanation in this regard since our studies have identified a number of BL patients who retain detectable LYDMA-specific T-cell surveillance7. The present work shows that in many cases of virus-associated BL, the emerging malignant clone is insensitive to such surveillance. Several EB virus-positive BL cell lines, recently established in vitro and expressing the class I histocompatibility locus antigens (HLAs) which restrict cytotoxic T-cell function, were not killed by HLA-matched LYDMA-specific effector populations in assays where the EB virus-positive lymphoblastoid cell line (LCL), derived from normal B cells of the same patient, sustained high levels of lysis.
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Rooney, C., Rowe, M., Wallace, L. et al. Epstein–Barr virus-positive Burkitt's lymphoma cells not recognized by virus-specific T-cell surveillance. Nature 317, 629–631 (1985). https://doi.org/10.1038/317629a0
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DOI: https://doi.org/10.1038/317629a0
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