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Correlation between Adriamycin-induced Augmentation of Interleukin 2 Production and of Cell-mediated Cytotoxicity in Mice¹

Grace Cancer Drug Center, Roswell Park Memorial Institute, New York State Department of Health, Buffalo, New York 14263 [M. J. E., D. M., K. R., E. M.], and Department of Medicine, SUNY at Buffalo, Buffalo General Hospital, Buffalo, New York 14203 [S. A. C.]

Based on the observation that spleen cells from Adriamycin-treated mice could develop augmented levels of cytotoxic T-lymphocyte activity in response to heat-treated and/or X-irradiated alloantigens, it was postulated that modulations in soluble mediators could be involved in this phenomenon. In fact, in this study Adriamycin-induced increases in the levels of prostaglandin E₂ and interleukin 2 activity have been observed with isolated cells. The "interleukin 2-like" activity was indistinguishable from that of partially purified interleukin 2 in terms of ability to restore responsiveness to experimentally inhibited primary alloantigen response cultures and to maintain long-term cultures of activated T-cells. Furthermore this latter activity was completely ablated by antiinterleukin 2 monoclonal antibody. While the modification in prostaglandin E₂ production did not appear to play a role in determining augmentation of cytotoxic T-cell activity, the modification in interleukin 2 production was consistent with the posibility that this is a primary mechanism of Adriamycin-induced augmented cell-mediated cytotoxicity.

¹ This work was supported by USPHS Grants CA15142, CA24538, and CA28835 awarded by the National Cancer Institute, Department of Health and Human Services.

² To whom requests for reprints should be addressed, at Grace Cancer Drug Center, Roswell Park Memorial Institute, 666 Elm St., Buffalo, NY 14263.

³ Present address: Department of Experimental Therapeutics, Cancer Research Institute, Kanazawa University, 13-1 Takaramachi, Kanazawa, 920 Japan.

Received 7/11/85. Revised 9/12/85. Accepted 9/16/85.