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Marked Reduction of Subcutaneous Tumor Growth by Intraperitoneal Administration of Recombinant Human Interleukin 2 with a Cell Accumulator, Proteose-Peptone, in Mice¹

Department of Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812 [H. U., K. T., K. N.], and Central Research Division, Takeda Chemical Industries, Ltd., 2-17-85, Jusohonmachi, Yodogawa-ku, Osaka 532 [S. T.], Japan

The growth of 3-methylcholanthrene-induced fibrosarcomas, Meth 1 and Meth A, was strongly suppressed by a combination of recombinant human interleukin 2 (rIL-2) with proteose-peptone (PP) administered i.p. to syngeneic mice. When 1 ml of 10% PP was injected i.p. on Day 6 followed by rIL-2 (50 µg) administered i.p. on Days 7 and 8 after the s.c. inoculation of tumor cells into female BALB/c mice, the tumors regressed. A similar result was also obtained when 12.5 µg of rIL-2 were injected on Days 7, 8, and 9 after s.c. inoculation of Meth 1 cells. The treatment with an anti-asialo-GM1 antibody had no effect on the regression of the Meth 1 tumor induced by the combination. However, the combined treatment with rIL-2 and PP did not suppress the growth of the Meth 1 tumor in adult thymectomized, irradiated, and fetal liver cell-reconstituted BALB/c mice. Therefore, this suggests that the T-cells might be the principal effectors of this antitumor system. The cytolytic activity of splenocytes and peritoneal exudate cells from Meth 1 tumor-bearing mice against Meth 1 cells was significantly augmented by the combined treatment. This peritoneal exudate cell also showed cytolytic activity against other target cells such as Meth A, antigenically distinct from Meth 1, YAC-1, a leukemic cell line sensitive to natural killer cells, and EL-4, a lymphoma cell line resistant to natural killer cells. The cytolytic activity of these effectors was reduced by the treatment with anti-thy1.2 antibody plus complement. The adherent cells in this peritoneal cavity had only a small cytolytic activity on Meth 1 and Meth A targets. The mechanism of antitumor immunity by rIL-2 in combination with PP and the therapeutic availability of this lymphokine are discussed.

¹ This work was supported by a Grant-in-Aid from the Ministry of Health and Welfare for Comprehensive 10-Year Strategy for Cancer Control, Japan.

² To whom requests for reprints should be addressed.

Received 11/ 9/87. Revised 6/ 1/88. Revised 9/13/88. Accepted 10/12/88.