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Updated: Aug 9, 2026

Isolation of Peritoneum-derived Mast Cells and Their Functional Characterization with Ca2+-imaging and Degranulation Assays
Published on: July 4, 2018
Monomeric human IgE evokes a transient calcium rise in individual human neutrophils
K S Collison1, A A Kwaasi, R S Parhar
1Biological and Medical Research Department, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Insights
Monomeric immunoglobulin E (IgE) binding to human neutrophils triggers intracellular calcium release, initiating a biological response. This response occurs without receptor cross-linking, suggesting IgE binding alone is sufficient.
Area of Science:
- Immunology
- Cellular Biology
- Biochemistry
Background:
- Human neutrophils play a critical role in immune responses.
- Immunoglobulin E (IgE) is involved in allergic reactions and immune defense.
- Intracellular calcium signaling is a key mechanism in cell activation.
Purpose of the Study:
- To investigate the primary biological responses of human neutrophils to monomeric IgE.
- To elucidate the signaling pathways involved in IgE-mediated neutrophil activation.
- To determine if IgE binding alone is sufficient to elicit a response.
Main Methods:
- Digital fluorescence calcium imaging was employed to monitor intracellular calcium levels.
- Neutrophils were treated with monomeric IgE.
- Pertussis toxin was used to investigate signaling pathways.
- Responses were compared to those induced by formyl-Met-Leu-Phe.
Main Results:
- Monomeric IgE induced a transient rise in intracellular calcium in human neutrophils.
- This calcium increase was inhibited by pertussis toxin.
- The calcium release originated from intracellular stores sensitive to formyl-Met-Leu-Phe.
- The IgE-induced calcium transient was independent of Fc gamma and Fc epsilon receptor ligation.
Conclusions:
- The binding of monomeric IgE to human neutrophils is sufficient to evoke a biological response.
- This response involves intracellular calcium release via a pertussis toxin-sensitive pathway.
- IgE-mediated neutrophil activation does not require Fc receptor cross-linking.
Abstract:
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.
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