Cytotoxicity of autologous Epstein-Barr virus-transformed cells mediated by interleukin-2 dependent, long-term T cell cultures is augmented by beta, but not alpha, recombinant interferon.

The immunomodulatory effect of two highly purified recombinant human interferons (IFN) on T cell-mediated cytotoxicity of autologous Epstein-Barr virus-transformed B cells (EBV-LCL) was assessed. Interferon beta ser, but not alpha 76, potentiated the destruction mediated by interleukin-2 (IL-2) dependent, long-term T cell cultures. The degree of potentiation of specific cytotoxicity was dependent on the concentration of the exogenously added IFN beta ser. In contrast to the potentiation of T cell-mediated cytotoxicity, IFN beta ser and alpha 76 did not modulate the cytotoxic activity of cytotoxic T cell clones that are specifically reactive to autologous EBV-LCL. These results indicate that the selective potentiation of EBV-LCL-reactive T cell-mediated cytotoxicity by IFN beta ser may not be due to a direct IFN effect on the cytotoxic T cells (CTLs) themselves. Rather, our results are consistent with IFN beta ser augmenting cytotoxic T cell reactivity indirectly, possibly via its influence on other immunoregulatory cells. Although the precise mechanism whereby IFN beta ser may potentiate cytotoxicity is not yet defined, the synergistic action of IFN beta ser and IL-2 on long-term CTL cultures offers an alternate means to selectively enhance a desirable cytotoxic response.