Humoral and cellular immunity to EBV and lymphoid cell line antigens in human lymphoma.

Although elevated antibody levels to the Epstein-Barr virus (EBV) have been reported in a number of lympho-proliferative neoplasms, it has not been possible to determine whether these antibodies were the result of a specific response to an oncogenic agent (EBV), whether they were a non-specific humoral compensation for depressed cell-mediated immunity (CMI), or whether a different mechanism was responsible. We have previously shown in a group of lymphoma patients that depressed cellular immunity to a number of standard antigens (Candida, SKSD, etc.) is not associated with an increase in antibody to EBV. In this study, we tried to compare CMI to possible EBV and lymphoid cell line antigens with humoral antibody to EBV. The two basis CMI assays utilized were lymphocyte cytotoxicity (LC) and skin testing (ST) for delayed hypersensitivity. In the LC assay, an EBV-containing cell line (F265) was used as the target. Reactivity against F265 was stronger in normal individuals than in cancer patients, suggesting a relationship to general cellular immune competence. ST studies showed that membrane extracts from lymphoid cell lines derived from patients with Burkitt's lymphoma and nasopharyngeal carcinoma (NPC) were more likely to elicit a delayed hypersensitivity in lymphoma and NPC patients than cell lines derived from normal individuals. Patients with ST reactivity against the membrane preparations from the tumour-derived cell lines were as likely to have elevated EBV antibodies as patients without such reactivity. The data strongly indicated that the elevated EBV titres in lymphoma patients are not related to a specific or non-specific depression of CMI.