Neutrophil-mediated cellular cytotoxicity triggered by immobilized aggregated IgG: an in vitro model of cell injury during immune complex diseases.

Normal human neutrophils were found to destroy ox red blood-cell targets when incubated on micropore filters coated with aggregated IgG, as determined by the 51Cr release method. An intact neutrophil oxidative metabolism was essential for the cytotoxic event, since cells from patients with chronic granulomatous disease failed to exert any cytolysis. The target-cell destruction was prevented by catalase, azide, and cyanide and was enhanced by superoxide dismutase, suggesting involvement of the myeloperoxidase-hydrogen peroxide system. Neutrophil-mediated cytotoxicity was markedly amplified by the chemotactic peptide N-formyl-methionyl-leucylphenylalanine, as a result of an increased activity of the myeloperoxidase-hydrogen peroxide cytolytic system itself. This system of cytotoxicity provides a direct evidence for the neutrophil capacity of destroying bystander target cells under conditions simulating the in vivo immunologically mediated tissue injury and offers an excellent model to study events occurring during immune complex diseases.