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.
Davies
E V
EV
Department of Surgery, University of Wales College of Medicine, Heath Park, Cardiff, UK.
Hallett
M B
MB
D000098:Acetophenones / Q000494:pharmacology; D000936:Antigen-Antibody Complex / Q000276:immunology*; D002118:Calcium / Q000097:blood*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects; D002478:Cells, Cultured; D006801:Humans; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D009532:Nickel / Q000494:pharmacology; D015398:Signal Transduction / Q000276:immunology*
D000098:Acetophenones; D000936:Antigen-Antibody Complex; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009532:Nickel; C006821:4-bromophenacyl bromide; D002118:Calcium