Rapid killing of actinomycin D-treated tumour cells by mononuclear phagocytes: reactivity in mouse strains with defective classical tumour cytotoxicity.

In confirmation of previous data, macrophages from C3H/HeJ, C57BL/10ScCR and A/J mice, exposed in vivo to BCG or in vitro to lymphokines, had little tumoricidal activity, as assessed in a 48-hr [3H]thymidine release assay against TU5 tumour cells, compared to macrophages from C3H/HeN, C57BL/6 and (BALB/c X DBA/2)F1 mice. Macrophages from these mouse strains were examined for their capacity to kill actinomycin D-pretreated WEHI 164 sarcoma cells in a 6-hr 51chromium release assay (drug-dependent cellular cytotoxicity, DDCC). Peptone-elicited macrophages from C3H/HeN, C57BL/6, (BALB/c X DBA/2)F1, C57BL/10ScCR and A/J mice had high DDCC activity, whereas C3H/HeJ macrophages expressed little cytotoxicity against actinomycin D-pretreated WEHI 164 cells. In vivo exposure to BCG or inactivated streptococci caused a modest augmentation of the DDCC effector function of C3H/HeJ macrophages, but levels of reactivity remained 20-fold less than those of similarly treated normal mice. Thus, C57BL/10ScCR and A/J macrophages have defective classical direct cytotoxicity but mediate DDCC efficiently, whereas C3H/HeJ macrophages are defective in both effector functions.