EFFECTS OF PROTEIN-KINASE INHIBITORS ON THE STIMULATED NEUTROPHIL RESPONSES BY DEGRADED IMMUNOGLOBULIN-G

Effects of protein kinase C inhibitors, staurosporine and 1-(5-isoquin olinylsulfonyl)-2-methylpipeazine dihydrochloride and protein tyrosine kinase inhibitors, genistein, tyrphostin and 2,5-dimethylcinnamate on the neutrophil responses stimulated by immunoglobulin G (IgG), comple ment C5a or platelet-activating factor were studied. After receptor bi nding, the role of protein kinase C and protein tyrosine kinase in the stimulation of neutrophil responses, superoxide production and lysoso mal enzyme release in degraded IgG-activated neutrophils may be simila r to chemoattractant-stimulated cells. In contrast to complement C5a o r platelet-activating factor, protein tyrosine kinase appears to play an important role in the regulation of intracellular Ca2+ mobilization in neutrophils activated by degraded IgG rather than by protein kinas e C.