1. IgE and Allergic Disease
IgE antibody was identified in 1967 as the molecular gatekeeper which controls the elicitation of allergic symptoms in humans [1,2]. Antibodies of the IgE isotype are produced by B-cell lymphocytes as a result of the exposure of a genetically-predisposed individual to any of hundreds of allergenic sources. Once produced, IgE antibodies circulate in the blood and bind onto high affinity epsilon specific receptors on mast cells in the skin and basophils in the blood. At this point, an individual can be considered sensitized (IgE antibody-positive) to the particular allergen specificity, although they may not manifest any allergic symptoms [3]. Repetitive allergen exposure induces a heightened immune response with an increase in IgE antibody levels in the blood. At the point where a critical mass of IgE antibody binds to the surface of an individual’s mast cells and basophils, allergen that is inhaled, ingested or injected into the body produces cross-links of surface bound antibodies sufficient to cause mast cells and basophils to become activated and release stored histamine and produce new vasoactive leukotriene mediators. The location of the release of histamine and leukotrienes in the body determines the location (skin, lung, gastrointestinal tract, systemic) and magnitude (severity) of the allergic symptom(s). Localized release in the skin can cause itching, swelling and redness. In contrast, systemic release of mediators can cause anaphylaxis, in some cases leading to death [4].