Perspective explaining the specificity of the recruitment of these cells (14–16). Interestingly, eotaxin can induce increased binding of eosinophils under shear force to endothelium via β1 and β2 integrin–mediated mechanisms, suggesting that eotaxin can affect several aspects of eosinophil migratory functions (17). In human asthma, eotaxin is produced at high levels and localized to the airway epithelium. This concentrated expression may preferentially target eosinophils to the epithelium and induce degranulation leading to the release of epithelium-damaging proteins. In addition to recruiting and activating eosinophils, eotaxin can effect other cell populations. Basophils degranulate in the presence of eotaxin, while Th2-type cells can migrate toward eotaxin. Thus, eotaxin may be a primary target for therapeutic intervention. A number of other chemokines and their receptors may also provide significant targets for therapeutic intervention because of their ability to recruit and activate other important cell populations into and around the airway. These chemokines and their receptors are discussed below.