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IgE alone-induced actin assembly modifies calcium signaling and degranulation in RBL-2H3 mast cells

Tatsuya Oka1, Masatoshi Hori, Akane Tanaka

  • 1Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo 113-8657, Japan.

American Journal of Physiology. Cell Physiology
|September 19, 2003
PubMed

Insights

Immunoglobulin E (IgE) alone triggers mast cell degranulation and calcium release. Low IgE concentrations induce actin assembly, acting as a negative feedback mechanism in mast cell signaling.

Area of Science:

  • Immunology
  • Cell Biology
  • Signaling Pathways

Background:

  • The role of immunoglobulin E (IgE) binding to its high-affinity receptor (FcεRI) in mast cell activation is typically viewed as passive.
  • Mast cell degranulation is a critical process in allergic responses.

Purpose of the Study:

  • To investigate the effect of IgE alone, without antigen stimulation, on mast cell degranulation.
  • To explore the role of actin dynamics in IgE-mediated mast cell activation.

Main Methods:

  • Treatment of rat basophilic leukemia (RBL)-2H3 mast cells and bone marrow-derived mast cells with monomeric IgE.
  • Measurement of cytosolic Ca2+ levels ([Ca2+]i) and degranulation.
  • Assessment of filamentous actin content and the effect of cytochalasin D on IgE-induced actin assembly.

Main Results:

  • Monomeric IgE alone, at concentrations of 500-5,000 ng/ml, increased [Ca2+]i and induced degranulation in both RBL-2H3 and bone marrow-derived mast cells.
  • At lower concentrations (5-50 ng/ml), monomeric IgE alone induced filamentous actin assembly in RBL-2H3 cells, without causing degranulation.
  • Cytochalasin D inhibited IgE-induced actin assembly, but IgE alone still increased [Ca2+]i and induced degranulation in treated cells.

Conclusions:

  • IgE alone can directly increase cytosolic Ca2+ levels and trigger degranulation in mast cells.
  • IgE induces actin assembly at sub-degranulatory concentrations, suggesting a negative feedback role in mast cell calcium signaling and degranulation.

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