The mechanism of regression of a rat macrophage-like tumor, AK-5 in syngeneic hosts is studied. Tumor rejecting animals produce antitumor antibodies which are cytotoxic to AK-5 cells in the presence of complement. About 30-50% of the animals do not develop the tumor when immune spleen cells are used in adoptive transfer of immunity assays. The cytotoxicity of immune spleen cells is totally lost on treating the effector cell fraction with anti-Thy. 1 and complement, indicating the involvement of thy. 1 positive cells in the rejection of AK-5. OX-8 (CD8) positive subset of natural killer cells is cytotoxic to AK-5 cells in vitro in the presence of anti-AK-5. Effector cells, when treated with either OX-8 or SH-34 (anti-asialo-GM1) monoclonals and complement, lost the cytotoxic activity against AK-5 cells suggesting the role for OX-8+ NK cells in the tumor regression. Effector cells were CD, negative since anti CD3 antibody, did not stain these cells. The animals which have rejected the tumor are immune to the subsequent tumor challenges with AK-5, however, other tumors do grow in these animals. This study demonstrates the efficiency of a multipronged attack launched by the host to overcome a rapidly growing tumor and therefore suggests a similar line of treatment for cancer immunotherapy.

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