Subversion of host defense mechanisms by murine tumors. II. Counter-influence of concomitant antitumor immunity.
Subcutaneous injection of murine tumor cells first resulted in a state of severely suppressed macrophage-mediated antibacterial resistance and then in a contrasting state of greatly enhanced antibacterial resistance. Whereas, the state of suppressed antibacterial resistance corresponded to a state of suppressed resistance to a tumor cell challenge, the generation of enhanced antibacterial resistance corresponded to the acquisition of concomitant antitumor immunity. It was suggested on the basis of this evidence that changes in the level of macrophage-mediated antibacterial resistance that occur during growth of the primary tumor reflected changes in the level of the host's resistance to the tumor itself. It was further suggested that the coincidental suppression of antibacterial and antitumor resistance that occurs during the initial stages of growth of the primary tumor represents the operation of a mechanism that enables the tumor to avoid destruction by macrophages. The results support the view that macrophages play an important role in native and acquired resistance to malignant tumors.
D000818:Animals; D000942:Antigens, Bacterial; D000951:Antigens, Neoplasm; D005260:Female; D007111:Immunity, Cellular; D007165:Immunosuppression Therapy; D008088:Listeriosis / Q000276:immunology; D008223:Lymphoma / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D008297:Male; D008325:Mammary Neoplasms, Experimental / Q000276:immunology; D051379:Mice; D009368:Neoplasm Transplantation; D009374:Neoplasms, Experimental / Q000276:immunology*; D012513:Sarcoma, Experimental / Q000276:immunology; D013997:Time Factors; D014184:Transplantation, Homologous
D000942:Antigens, Bacterial; D000951:Antigens, Neoplasm