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Effect of Recombinant Human Interferon-A/D on in Vivo Murine Tumor Cell Growth¹

Department of Zoology, Faculty of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606 [K. U., S. S., K. I., M. K., K. N., T. K., Y. Y., S. M.] and Kyoto Pasteur Institute 425, Yamamoto-cho, Gokomachi-dori, Oshikojiagaru, Nakagyo-ku, Kyoto 604 [K. U.], Japan

We investigated the effect of human recombinant interferon-A/D (A/D-IFN), which is known to delay the growth of murine tumor cells, on the growth of S1 and R1 subline cells of murine Meth A fibrosarcoma in the peritoneal cavity of mice. In vitro growth of S1 cells was sensitive to, and that of R1 cells was resistant to, the direct effect of A/D-IFN, as with murine natural IFN-/ß, which was used originally to isolate these sublines. In vivo, however, the growth of not only S1 cells but also R1 cells was suppressed by the administration of A/D-IFN, and the survival time of tumor-bearing mice was prolonged. Although A/D-IFN had a direct effect on S1 cells in vivo, R1 cells were susceptible only to the indirect effect via the host cells. Macrophages (Mø) harvested from the peritoneal cavity of A/D-IFN-treated mice bearing ascitic R1 cells were very effective in suppressing the in vitro growth of R1 cells; those from non-R1-bearing A/D-IFN-treated mice were less effective. The results of in vitro experiments indicate that Mø are very probably activated by the synergism of A/D-IFN and Mø-activating factor(s) produced by lymphoid cells in tumor-bearing mice.

¹ This work was supported by a Grant-in-Aid for Cancer Research from the Ministry of Education, Science and Culture of Japan, and a Shimizu Foundation Research Grant.

² To whom requests for reprints should be addressed, at Department of Zoology, Faculty of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-Ku, Kyoto, 606 Japan.

Received 2/16/87. Revised 8/10/87. Revised 1/11/88. Accepted 1/22/88.