The allergic response is a highly complicated and multifaceted dysfunction of the immune system. Designed to protect against dangerous invaders such as pathogenic organisms, the results of the allergic response, when mobilized against harmless foreign (or even autogenous) substances, can be disastrous. Immune function is the most recondite system of integrated functions of which we have any understanding, exceeding all but the brain in complexity. Among the more important single mechanisms of allergic reactivity is the pathway that leads to the release of histamine. IgE antibody programmed to interact with specific antigens is produced by lymphoid tissue and binds to IgE receptors (FC[epsilon]RI and FC[epsilon]RII) on several cell types, notably mast cells. FC[epsilon]RI is the major receptor, while FC[epsilon]RII is a minor one. When these cell-bound antibodies encounter their programmed allergen, they set off a chain reaction inside the cell that stimulates production of quantities of inflammatory chemicals–interleukins, leukotrienes, and histamine. These chemicals then bring about the many manifestations of the allergic/inflammatory reaction. The acute effects are tissue swelling and mucus membrane weeping from leaky capillaries, increased blood flow from dilated blood vessels, pain from noxious stimulation of afferent nerves, bronchial smooth muscle spasm, and, in severe cases, falling blood pressure and respiratory compromise. Chronic effects include damaging tissue remodeling–brosis, hyperplasia, and polyp formation–also from the effects of the same chemicals. (1,2) A number of therapeutic interventions attempt to modulate these reaction pathways. Foremost among them are antihistamines, since histamine is so central to the entire process, but many other chemicals also are used. Corticosteroids, sympathomimetics, leukotriene antagonists, antibodies to IgE, and other inflammatory cytokines are the pharmaceutical foundation of allergy treatment, even though they all have significant side effects.