Epstein-Barr virus-positive Burkitt's lymphoma cells not recognized by virus-specific T-cell surveillance.
The pathogenesis of Epstein-Barr (EB) virus-positive Burkitt's lymphoma (BL) appears to involve the combined actions of virus-induced B-cell proliferation, and 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 process. 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 carriers. Immunosuppression, such as that which malarial infection may induce, 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 surveillance. 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.
D000954:Antigens, Surface / Q000276:immunology*; D002051:Burkitt Lymphoma / Q000276:immunology* / Q000382:microbiology; D002460:Cell Line; D006680:HLA Antigens / Q000032:analysis*; D004854:Herpesvirus 4, Human / Q000302:isolation & purification*; D006801:Humans; D016169:Lymphocyte Function-Associated Antigen-1; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*
D000954:Antigens, Surface; D006680:HLA Antigens; D016169:Lymphocyte Function-Associated Antigen-1