EBV Infection of B-CLL Cells in vitro Potentiates Their Allostimulatory Capacity if Accompanied by Acquisition of the Activated Phenotype

Abstract

The immune response is mainly responsible for the harmless EBV carrier state in humans, as indicated by the elevated risk for virus genome carrying B cell malignancies in immunosuppressed individuals (Nalesnik et al. 1988). The role of cellular immunity in the control mechanism is substantiated by in vitro results showing that T cells can inhibit the virus induced transformation of B cell cultures and that cytotoxic T cells (CTL) specific for autologous immortalized B cells (lymphoblastoid cell lines, LCLs) are detected in experiments performed with cells of seropositive individuals (Thorley-Lawson et al. 1977; Moss et al. 1979). In search of the CTL targets, all the known EBV encoded proteins expressed in LCLs, except for one, EBNA-1, provided peptides which were recognized by T cells when presented by the appropriate HLA molecules on the cell surface (Masucci and Ernberg 1994). These CTLs represent an EBV specific cellular memory because they can be generated in vitro only in experiments performed with lymphocytes of seropositive individuals (Moss et al. 1979). On the other hand, autologous LCL can stimulate T lymphocytes in vitro even in experiments with cells of seronegative individuals (Weksler 1976). It is likely that the efficient interaction of EBV genome carrying B cells with T lymphocytes is important in controlling their proliferative potential prior to development of the specific immunity.