ROLE OF THE OXIDATIVE METABOLIC BURST IN THE ANTIBODY-DEPENDENT CELLULAR CYTO-TOXICITY MEDIATED BY NEUTROPHIL POLYMORPHONUCLEARS

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  • 1 January 1982
    • journal article
    • research article
    • Vol. 10  (10) , 859-866
Abstract
The mechanisms by which [human] neutrophil polymorphonuclears (PMN) mediate antibody-dependent cellular cytotoxicity (ADCC) were studied. Under experimental conditions which allow target cell phagocytosis, PMN efficiently kill IgG-sensitized ox erythrocytes, as determined by the 51Cr release assay. Inhibition of the target cell ingestion by colchicine did not affect the PMN cytotoxic activity, suggesting that target cell phagocytosis does not represent an essential step in the PMN-mediated ADCC against erythrocytes. PMN from patients with chronic granulomatous disease, who have defective oxidative metabolic burst, displayed an impaired ADCC activity, which was unaffected by changes in the phagocytic capacities induced by colchicine. Under the experimental conditions employed, both the intracellular and the extracellular target cell destruction by PMN involve oxygen-dependent mechanisms.