Journal of Leukocyte Biology 39:205-221 (1986) Rapid Killing of Actinomycin D-Treated Tumor Cells by Mononuclear Phagocytes: Characterization of Effector Cells in Mice

tumor cells susceptible to killing by mouse resident or peptone-induced pen-toneal exudate cells (PEC) in a 6-hr 51Cr release assay. Cytotoxicity was attributed to cells of the monocyte macrophage lineage on the basis of tissue distribution, separation by adherence on plastic and carbonyl iron, membrane antigens, and expression in mice with defecti’.e I cell- or NK cell-mediated immunity. Macrophages from four strains of mice (C3H/HeJ, NJ, P/J, C57BI/ 10 ScCR) previously shown to have defective “classical ” nonspecific tumoricidal activity were examined for killing of Act-D-treated WEHI 164 cells. C3H/HeJ peritoneal macrophages had little or no DDCC, whereas cells from NJ, P/J, and CS7BI/10 ScCR mice had normal levels of this reactivity. Tumor cells exposed to ActD were heterogenous in their susceptibility to killing by PEC, with five lines showing significant, though variable, lysis, whereas 12 tumor lines, normal fibroblasts, and lymphoblasts were not appreciably killed under the same conditions. Macrophage-mediated DDCC was also detectable in a colony assay. DDCC could explain how macrophages contribute to the antitu-mor activity of selected chemotherapeutic agents in murine tumor models. Key words: actinomycin 0, murine macrophage, cytotoxicit