In order to analyze the components of EBV-specific immunological memory that contribute to the T-cell-mediated inhibition of EBV-induced B-cell transformation, we have investigated the growth inhibitory potential of T cells cultured for 3 days with B cells exposed to transforming and nontransforming EBV preparations. T cells cultured for 3 days with EBV-infected autologous B cells inhibited the transformation of newly infected 6 lymphocytes. T cells cultured with the virus, with autologous uninfected B cells, or in the presence of 10 ,ugh1 Con-A had a significantly weaker inhibitory capacity. The inhibitory capacity was induced by co-cultivation with B cells infected with the transforming 895-8 virus strain, with the non-transforming P3HRI virus strain, and also with UV-inactivated 895-8 virus. B-cells infected with transforming 895-8 virus induced the strongest growth inhibitory activity. Activation of the T cells was shown by their IL-2 production, proliferation, and generation of non-specific cytotoxicity. These results suggest that the initial event of the Tcell response in EBV-infected cultures is induced by antigens associated with the viral particles presented by B lymphocytes. 'To whom reprint requests should be addressed. inson i t al., 1981a,b).
The decisive events in the in vitro triggering of T-cell growth-inhibitory potential seem to occur ea;'iy afrer confrontation with EBV-infected B cells. The immunosuppressive