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Monomeric human IgE evokes a transient calcium rise in individual human neutrophils
Author(s) -
Collison Kate S.,
Kvvaasi Aaron A.A.,
Parhar Ranjit S.,
AlSedairy Sultan T.,
AlMohanna Futwan A.A.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.4.459
Subject(s) - immunoglobulin e , pertussis toxin , biology , calcium , receptor , chemotaxis , calcium in biology , immunology , transient receptor potential channel , intracellular , microbiology and biotechnology , antibody , biochemistry , medicine , g protein
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 Fcγ receptors and of Fc 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.