Abstract
3-Deazaadenosine (3-DAA), an inhibitor of S-adenosyl-L-homocysteine hydrolase, caused a dose-dependent inhibition of antibody-dependent cellular cytotoxicity (ADCC) against erythrocyte target cells of mouse spleen effector cells and complete Freund's adjuvant-induced peritoneal exudate cells. Inhibition of ADCC was accompanied by a proportional augmentation of antibody-dependent phagocytosis (ADØ). When resident peritoneal cells were used as the source of effectors, ADØ was inhibited by 3-DAA without augmentation of ADCC. Long-term (overnight) preincubation studies showed that the effect of 3-DAA wi peritoneal ADØ increased with time and was irreversible. Peritoneal exudate cells elicited by sodium caseinate mediated both antibody-dependent and -independent (spontaneous) phagocytosis. 3-DAA was shown as a potent and irreversible inhibitor of spontaneous phagocytosis. Inhibition of phagocytosis in these cell preparations resulted in augmentation of ADCC. In most of these effector cell populations, effects of 3-DAA were potentiated by the presence of L-homocysteine thiolactone.
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