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Related Experiment Videos

IgE and inflammatory cells.

A Capron1, M Capron, C Grangette

  • 1Centre d'Immunologie et de Biologie Parasitaire, Unité Mixte INSERM U 167-CNRS 624, Institut Pasteur, Lille, France.

Ciba Foundation Symposium
|January 1, 1989
PubMed
Summary
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Immunoglobulin E (IgE) antibodies bind to inflammatory cells via Fc epsilon RII receptors, triggering mediator release. This interaction is crucial for parasite defense and allergic reactions.

Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • Immunoglobulin E (IgE) antibodies play a role in defense against parasites and in allergic reactions.
  • Specific surface receptors, Fc epsilon RII, mediate IgE antibody interactions with inflammatory cells.
  • Genes for IgE receptors on B cells and eosinophils have been cloned, revealing structural homologies and potential heterogeneity.

Purpose of the Study:

  • To explore the role of IgE receptors (Fc epsilon RII) on inflammatory cells in mediating effector functions.
  • To investigate the molecular structure and heterogeneity of IgE receptors.
  • To understand the mechanisms of IgE-mediated cell activation and mediator release.

Main Methods:

  • Studies in parasitic disease models.

Related Experiment Videos

  • Gene cloning of IgE receptors.
  • Molecular structure analysis of Fc epsilon RII.
  • Investigation of eosinophil and platelet activation.
  • Detection of released mediators using chemoluminescence and electron magnetic resonance.

    • Main Results:

    • IgE antibodies interact with mononuclear phagocytes, eosinophils, and platelets via Fc epsilon RII receptors.
    • Eosinophil IgE receptors share structural similarities with B cell receptors but may exhibit heterogeneity.
    • Eosinophil IgE receptors contain sequences common to adhesion proteins.
    • Antigen binding to IgE triggers effector functions, including the release of eosinophil peroxidase.
    • Platelet activation by IgE leads to the production of oxygen-derived free radicals and cytocidal effects.

    Conclusions:

    • IgE receptors on inflammatory cells are critical for initiating cell effector functions.
    • These interactions are vital in both host defense against parasites and the pathogenesis of allergic reactions.
    • Further research into IgE receptor heterogeneity may reveal new therapeutic targets.