Impairment of systemic concomitant antitumor immunity by excess soluble tumor antigen

Abstract

Animals bearing a 3-methylcholanthrene induced sarcoma called MC1 rejected substantial numbers of a suspension of the same tumor cells injected IV in comparison with normal rats. The factors that protected the host against lung metastases were impaired by the administration of tumor antigen in the form of irradiated tumor cells or soluble tumor antigen. Animals bearing an MC1 tumor which received either unrelated MC11 irradiated tumor cells or soluble tumor antigen had more lung metastasis than the animals not given any tumor products. However, a statistically significant increase in the number of lung tumor nodules was observed in the rats treated with MC1, compared with those treated with MC11 tumor antigen (soluble tumor antigen or irradiated tumor cells) or no tumor antigen. The increase in the outgrowth of lung tumor nodules in the tumor-bearing host given an excess of tumor materials was produced by a dual mechanism of inhibition of the concomitant immune resistance and nonspecific resistance. The present study shows that soluble tumor antigen similar to material shed from a primary tumor is able to impair concomitant immune resistance to tumor cells within the lungs.