A novel pathway for Ca2+ signalling in neutrophils by immune complexes

The data presented here demonstrates that immune complexes use novel routes for stimulating a two-phase rise in cytosolic-free Ca2+ concentration. The initial transient Ca2+ rise resulted from release of Ca2+ from intracellular stores, by a route which, unlike f-met-leu-phe, was inhibited by bromophenacyl bromide. The second phase resulted from transmembrane influx and occurred in the absence of store release and by Ca2+ channels that were inhibited by Ni2+ but not SKF 96365 or econazole. Stimulation by immune complexes therefore involves novel routes for both the release of stored Ca2+ and the opening of Ca2+ channels in the plasma membrane.