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MacDonald SM, Lichtenstein LM, Proud D, et al. Studies of IgE dependent histamine releasing factors: heterogeneity of IgE. J Immunol 1987;139:506. Siriganian RP. Mechanism of IgE-mediated hypersensitivity. In: Middleton E, Reed CE, Ellis EF, et al, eds. Allergy: principles and practice. 4th ed. St. Louis: CV Mosby, 1993. Dvorak AM, Morgan ES. Ribonuclease-gold ultrastructural localization of heparin in isolated human lung mast cells stimulated to undergo anaphylactic degranulation and recovery in vitro.

The number and type of mast cell mediator interactions are potentially enormous, and their pathobiologic consequences are relevant to a variety of homeostatic and disease processes. The best clues to the interaction of mediators are the known physiologic and pathologic manifestations of allergic diseases. It is hoped that the valuable tool of gene knockouts in mice will elucidate critical individual and interactive roles of these molecules. THE ROLE OF THE MAST CELL AND ITS MEDIATORS IN TISSUE The most compelling evidence for the role of mast cells and mediators in human tissue is derived from experiments in which IgE-dependent mast cell activation in skin is caused by specific antigen (or antibody to IgE).

Interferon-g (IFN-g) is the most important inhibitor of IgE synthesis. CD154, the T-cell ligand for CD40 on the B cell, promotes IgE transcription through nuclear factor, NF-kB. Antigen presented to the T-cell receptor (TCR) by class II major histocompatibility complex molecules on the B cell initiates this complex process. (Adapted from, Cory DB, Kheradmand F. Induction and regulation of the IgE response. ) During terminal differentiation of IgE B cells to plasma cells producing IgE, IgE-binding factors have been described that either enhance or suppress IgE synthesis (28).

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Allergic Diseases by Patterson


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