The molecular and cellular mechanisms mediating the allergic inflammatory cascade involve multiple mediators, cell types, and pathways. Of particular interest are the pathways regulated by the T(H)2 lymphocyte, which result in release of IL-4 (important to IgE synthesis) and IL-5 (important to eosinophil proliferation). IL-4 regulates differentiation of naïve T(H)0 cells to develop a T(H)2 phenotype and stimulates B cells to produce IgE. Cross-linking by allergen of IgE affixed to high-affinity receptors on mast cells and basophils triggers degranulation and the release of preformed inflammatory mediators (important to the early phase response), and subsequently initiates synthesis and the release of lipid mediators and cytokines (which may contribute to the late phase response). Eosinophils may also play a prominent role in the development of bronchial hyperreactivity. IL-5, which is a lineage-specific eosinophil growth factor, increases the formation of eosinophils from progenitor cells and, in concert with CCR3 active chemokines, increases their trafficking to sites of allergic inflammation. An improved understanding of the basic mechanisms of allergic inflammation has led to the discovery of molecular targets involved in the initial events of the inflammatory cascade. Potential targets for the development of novel therapies for allergic disease include IgE, the T(H)2 lymphocyte, and T(H)2-derived cytokines, IL-4 and IL-5.