When cyclophosphamide was administered to mice before immunization with syngeneic SV40 transformed cells, the specific immune response elicited, as was measured by in vitro 51Cr release assay was stronger and lasted longer when compared to the response generated in noncyclophosphamide-treated mice. The augmentation effect of the drug was dependent on cyclophosphamide concentration being optimal at 100 mg/kg and on the time of drug administration in relation to antigen immunization being optimal at 2 d before antigen administration. Transfer of T cells from normal syngeneic mice to drug-treated animals abolished the cyclophosphamide-induced augmentation of immune response. These results implied that cyclophosphamide sensitive T cells suppressed the in vivo generation of specific effector T cells against SV40-induced tumor-associated antigens.
Lymphoid cells from many normal W/Fu rats reacted in a 51Cr release cytotoxicity assay against (C58NT)D, a syngeneic Gross leukemia virus-induced tumor. The reactivity was maximal in young rats at 5-8 weeks of age and rapidly declined thereafter. Within reactive rats, the cytotoxicity was widely distributed among the various lymphoid organs. Since immunization of W/Fu rats with (C58NT)D was shown to elicit specific cell-mediated cytotoxic reactivity, studies were done to compare the characteristics of the natural reactivity with those of the immune reactivity. The specificity of both types of reactivity was analyzed in detail by an inhibition assay. The natural and the immune reactivities appeared directed against antigens associated with rat endogenous type-C viruses. The major differences between the natural reactivity and immune reactivity were the nature of the effector cells. Whereas immune reactivity was T-cell dependent, normal reactivity was not affected by treatment with antisera against T cells plus complement. Natural effector cells were not adherent and did not have macrophage properties. The active cells also did not have receptors for Ig or complement. The absence of detectable cell-surface markers on the natural effector cells was seen in studies of natural cytotoxic reactivity of mice, and it is proposed that the natural cytotoxicity in both systems is mediated by a unique subpopulation of lymphoid cells, tentatively designated "N" cells.
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