Different requirements for the induction of antibody-dependent and immune complexes triggered cytotoxicity mediated by monocytes.
We have previously shown that immune complexes triggered nonspecific cytotoxicity (NSC) towards nonsensitized target cells and antibody-dependent cellular cytotoxicity (ADCC), two functions mediated through monocyte Fc gamma receptors, employing different lytic mechanisms [Geffner, J. R., et al. (1986) Clin. Exp. Immunol. 67, 646]. In this report, we analyze some of the metabolic requirements involved in the induction of monocyte NSC and ADCC. The results showed NSC to be dependent on: (1) metabolic energy derived from glycolysis, (2) availability of external Ca2+, (3) calmodulin activity, (4) integrity of microtubules, but not the microfilament system, and (5) activation of phospholipase(s) and lipoxygenase. On the other hand, ADCC was not impaired by: (1) inhibition of glycolysis, (2) Ca2+ chelation, (3) disruption of microtubules, or (4) inhibition of calmodulin or lipoxygenase. It is concluded that monocyte NSC and ADCC are regulated by different endogenous signals.
D000920:Antibody-Dependent Cell Cytotoxicity; D000936:Antigen-Antibody Complex / Q000276:immunology; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D003599:Cytoskeleton / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D004734:Energy Metabolism; D006019:Glycolysis; D006801:Humans; D066298:In Vitro Techniques; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism; D010740:Phospholipases / Q000378:metabolism
D000936:Antigen-Antibody Complex; D001095:Arachidonic Acids; D016718:Arachidonic Acid; D010740:Phospholipases; D002118:Calcium