Monomeric human IgE evokes a transient calcium rise in individual human neutrophils.
Digital fluorescence calcium imaging was used to investigate and identify the primary biological responses of human neutrophils to monomeric immunoglobulin E (IgE). Treatment of neutrophils with IgE caused a transient rise in the level of intracellular calcium that was inhibited by pertussis toxin. The calcium rise was due mainly to release from an intracellular membrane-enclosed store that is also sensitive to the chemotactic peptide formyl-Met-Leu-Phe. The IgE-induced calcium transient was independent of Fc gamma receptors and of Fc epsilon receptor ligation. Our data suggest that the mere binding of IgE to neutrophils is sufficient to evoke a biological response without the need for IgE/receptor cross-linking.
Collison
K S
KS
Biological and Medical Research Department, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Kwaasi
A A
AA
Parhar
R S
RS
al-Sedairy
S T
ST
al-Mohanna
F A
FA
D000595:Amino Acid Sequence; D002118:Calcium / Q000097:blood*; D005110:Extracellular Space / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D005453:Fluorescence; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007073:Immunoglobulin E / Q000494:pharmacology*; D007424:Intracellular Fluid / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D008969:Molecular Sequence Data; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism* / Q000648:ultrastructure; D017452:Receptors, IgG / Q000502:physiology
D017452:Receptors, IgG; D007073:Immunoglobulin E; D009240:N-Formylmethionine Leucyl-Phenylalanine; D002118:Calcium