Activation of mast cells for mediator release through IgE receptors

T. Ishizaka, K. Ishizaka

Research output: Contribution to journalArticle

Abstract

Studies on immunoglobulin E (IgE) and the mechnisms of reaginic hypersensitivity reactions in the past 15 years revealed that IgE has high affinity for mast cells and basophil granulocytes and that the reaction of cell-bound IgE antibody with allergen induces the release of a variety of chemical mediators from the cells. Other immunoglobulins, such as IgG and IgA, do not combine with these cells or bind with much lower affinity and are incapable of mediating reaginic hypersensitivity reactions. The specific binding of IgE molecules to the target cells is due to unique structures in the Fc portion of IgE molecules and the presence of receptor sites for this structure on target cells. The binding of IgE to the receptors with high affinity does explain why a minute dose of IgE antibody is sufficient for sensitizing homologous tissues and why passive sensitization with IgE antibody is so persistent. It is generally accepted that histamine release from the target cells is triggered by bridging of cell-bound IgE molecules by multivalent ligand. It was not known, however, why bridging of cell-bound IgE molecules initiates the mediator release. A hypothesis was presented that polymerized IgE molecules may activate membrane-associated enzymes which lead to mediator release. However, comigration of IgE and receptors on the surface of target cells suggested the possibility that receptor molecules may be involved in triggering mediator release. As IgE molecules are firmly bound to receptors, bridging of cell-bound IgE molecules probably brings receptor molecules into close proximity. A hypothesis was therefore presented that such local changes in membrane structures or possible interaction between adjacent receptor molecules may induce activation of membrane-associated enzymes, and these biochemical processes lead to mediator release. In the past 4 years, a series of experiments was undertaken to prove this hypothesis. This article summarizes evidence for the role of IgE-receptors on mast cells in the triggering of mediator release, and reviews the activation of membrane-associated enzymes induced by bridging of IgE-receptors.

Original languageEnglish (US)
Pages (from-to)188-235
Number of pages48
JournalProgress in Allergy
VolumeVOL. 34
StatePublished - Jan 1 1984

ASJC Scopus subject areas

  • Immunology and Allergy

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