These diseases result from IgE-dependent release of mediators from sensitized basophils and mast cells upon contact with an offending antigen (allergen). Associated disorders include anaphylaxis (Chap. 28 Anaphylaxis), allergic rhinitis, urticaria, asthma, and eczematous (atopic) dermatitis.
IgE binds to the surface of mast cells and basophils through a high-affinity receptor. Cross-linking of this IgE by antigen causes cellular activation with subsequent release of preformed and newly synthesized mediators (Fig. 159-1. Bioactive Mediators of Three Categories Generated by Ige-Dependent Activation of Murine Mast Cells Can Elicit Common but Sequential Target Cell Effects Leading to Acute and Sustained Inflammatory Responses). These mediators have been implicated in many pathophysiologic events associated with immediate-type hypersensitivity, such as vasodilation, increased vasopermeability, smooth-muscle contraction, and chemotaxis of neutrophils and other inflammatory cells. The clinical manifestations of each allergic reaction depend largely on the anatomic site(s) and time course of mediator release.