Abstract

Natural killer (NK) cell activity was generated in the spleen of C3H/HeN mice by i.p. administration of poly I:C, while i.p. injection of BCG primarily promoted the generation of NK-like cells in peritoneal exudates (PE). A single injection of 10 mg of BCG 9 days before s.c. challenge with the MBT-2 murine bladder cancer was found to induce a 45% protection against tumor take. However, a single injection of 100 micrograms poly I:C 16 h before tumor cell challenge did not protect the animals against tumor take. Intratumoral injection of either PE cells from BCG-immunized or spleen cells from poly I:C-treated mice into mice developing tumor, was capable of suppressing tumor growth in vivo. The mean tumor diameters of these two experimental groups of animals on day 40 were significantly smaller (P less than 0.005) than in the controls, and they survived approximately 10 days longer than the controls. Since this in vivo tumor suppressive effect by the lymphoid cell population correlated with the increase in NK-like cell activity assayed in vitro, and most of the adherent cells had been removed before injection, it is suggested that the antitumor function of the lymphoid cell population may be mostly due to the presence of "activated" NK or NK-like cells. These results support the concept of NK therapy for cancer.

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