Dissociation between tumour resistance and delayed-type hypersensitivity to tumour-associated antigens in the mouse.
A comparison was made in mice between resistance to growth of a syngeneic methylcholanthrene-induced fibrosarcoma (Meth A) and specific delayed-type hypersensitivity to this tumour. Resistance could be induced in 90% of mice following a single injection of 10(4) Meth A cells. This resistance could be transferred by spleen cells but not serum. Delayed skin reactivity to ultrasonicated Meth A cells was found in both tumour-resistant and tumour-bearing mice and could be passively transferred by spleen cells and serum. These findings suggest a dissociation between tumour resistance and specific delayed-type hypersensitivity. It would appear that, in this system, delayed skin reactivity to Meth A tumour cells is mediated by humoral antibody despite a mononuclear cell infiltrate at 24 and 48 h and that this could be the reason for its lack of correlation with host resistance to tumour growth which is cell-mediated and not transferable by serum.
D000818:Animals; D000951:Antigens, Neoplasm / Q000276:immunology*; D003520:Cyclophosphamide / Q000494:pharmacology; D004306:Dose-Response Relationship, Immunologic; D005354:Fibrosarcoma / Q000276:immunology*; D006614:Hindlimb / Q000473:pathology; D006968:Hypersensitivity, Delayed / Q000473:pathology; D007113:Immunity, Innate; D007116:Immunization, Passive; D051379:Mice; D008807:Mice, Inbred BALB C; D012513:Sarcoma, Experimental / Q000276:immunology
D000951:Antigens, Neoplasm; D003520:Cyclophosphamide