The recruitment of eosinophils to sites of allergic inflammation is a complex process that is primarily regulated by inflammatory cytokines and chemokines. These molecules act in concert to stimulate peripheral eosinophilia, regulate homing of eosinophils to the inflammed organ, and promote eosinophil-vascular endothelium interactions, extravasation, chemotaxis, and localization to the site of the inflammatory stimulus. The essential and specific role of IL-5 in regulating blood and tissue eosinophilia, and the subsequent involvement of this leukocyte in the induction of lung damage and airway dysfunction identifies IL-5 as a primary therapeutic target. Developing strategies to inhibit IL-5 production and action, such as by the delivery of inhibitory cytokines to the lung, which specifically down-regulate CD4+ TH2 cell responses and eosinophilic inflammation, may be more beneficial than the current drugs of choice for preventive treatment and in the relief of acute and chronic asthma and allergic disease.