The efficacy of glucocorticoids in the treatment of allergic diseases is well established. Among their observed beneficial effects is the ability to reduce the appearance of eosinophils and eosinophil-derived mediators at sites of allergic inflammation. How glucocorticoids prevent eosinophil influx in vivo is not completely understood, but may include effects on various aspects of eosinophil recruitment. Studies examining the effects of glucocorticoids on (1) eosinophil survival, (2) eosinophil and endothelial adhesion responses, (3) the production of endothelial-activating and eosinophil-priming cytokines, and (4) eosinophil chemotactic factor responsiveness, will be reviewed. It is likely that the potent ability of glucocorticoids to prevent eosinophil emigration into tissue sites results from a combination of both direct and indirect effects on the eosinophil, the endothelium, and other cells involved in the production of pro-inflammatory mediators responsible for eosinophil infiltration.