ABSTRACT
The binding of immunoglobulin E (IgE) to high-affinity receptors on effector cells, such as mast cells and basophils, and the subsequent exposure to allergens initiates a cascade resulting in the release of proinflammatory mediators that contribute to the acute and chronic symptoms of allergic airway diseases. Importantly, anti-IgE treatment reduces the expression of FceRI receptors on basophils as shown in subjects with perennial allergic rhinitis with positive skin tests to dust mite. Anti-IgE concentrations were highest in the serum compartment, and no specific organ deposition was observed. The immune complexes were eliminated by urinary excretion. The one exception of a change in specific IgE was the high-dose anti-IgE group, which showed a marginally significant increase in average endpoint skin test titration allergen concentration. Allergen-specific immunotherapy is the only disease-modifying treatment for allergic airway diseases, and beneficial effects can be observed even years after discontinuation.
