Abstract
The effect of metabolic inhibitors and hormones on the susceptibility of P815 murine mastocytoma cells to antibody-C and cell-mediated killing, and on the ability of the cells to synthesize DNA, RNA, protein, carbohydrate, and lipid was tested. Pretreatment of the cells with adriamycin, actinomycin D, and puromycin increased the sensitivity of the cells to killing by rabbit anti-P815 antibody plus guinea pig C, but not by allogeneic P815-sensitized spleen cells. Conversely, mitomycin C treatment enhanced the cells' sensitivity to cell-mediated, but not antibody-C, killing. Insulin and hydrocortisone, but not epinephrine, were effective in decreasing the susceptibility of the cells to killing by both antibody-C and cell-mediated attack systems. The kinetics of the drug-induced increase and the hormone-induced decrease in susceptibility of the cells to antibody-C killing correlated with a decrease and increase, respectively, in the ability of the cells to incorporate fatty acid into complex cellular lipid. No such correlation was found between cellular lipid synthesis and tumor cell susceptibility to cell-mediated killing. The ability of the cells to resist either form of immune attack was not dependent on the ability of the cells to synthesize DNA, RNA, protein, or complex carbohydrate. These results suggest that the susceptibility of these tumor cells to antibody-C vs cell-mediated killing may be linked to different metabolic properties of the cells, and may reflect differences in the mechanisms of humoral vs cellular immune attack.
Published Version
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