The immunological basis of endotoxin-induced tumor regression. Requirement for a pre-existing state of concomitant anti-tumor immunity.
It was shown that of four syngeneic, murine tumors investigated, only those that evoked the generation of a state of concomitant anti-tumor immunity were susceptible to endotoxin-induced regression. Moreover, the temporal relationship between the generation of concomitant immunity and the onset of susceptibility to endotoxin-induced regression points to the likely possibility that tumor regression depends on the preceding acquisition of the specifically-sensitized, effector T cells that express concomitant immunity. It is suggested that endotoxin-induced hemorrhagic necrosis which invariably precedes tumor regression serves to create conditions inside the tumor that are conducive to the entry and the functioning of effector T cells. It is also suggested that tumor necrosis factor causes hemorrhagic necrosis rather than tumor regression.
D000818:Animals; D004731:Endotoxins / Q000494:pharmacology / Q000627:therapeutic use*; D005354:Fibrosarcoma / Q000276:immunology; D007109:Immunity / Q000187:drug effects; D007167:Immunotherapy; D008325:Mammary Neoplasms, Experimental / Q000276:immunology; D051379:Mice; D009374:Neoplasms, Experimental / Q000276:immunology / Q000628:therapy*; D012513:Sarcoma, Experimental / Q000276:immunology; D013268:Stimulation, Chemical; D013601:T-Lymphocytes / Q000276:immunology*
D004731:Endotoxins