Allergic inflammation is characterized by recruitment of specific leukocyte subpopulations from blood into tissue and requires a series of cell adhesion-molecule-mediated interactions between postcapillary vascular endothelium and the leukocyte cell surface. Three major groups are involved: selectins, integrins, and the immunoglobulin gene superfamily. P- and E-selectin mediate initial leukocyte adhesion, whereas beta 2-integrin/ICAM-1 and VLA-4/VCAM-1 pathways mediate leukocyte arrest and transendothelial migration. Because VLA-4 expression is restricted to eosinophils and lymphocytes, VCAM-1 has been implicated in selective eosinophil recruitment characterizing allergic inflammation. However, additional factors such as profile of cytokine release are likely to operate since tissue eosinophilia has been observed in the absence of VCAM-1 expression. Recent use of monoclonal antibodies against functional epitopes on various cell adhesion molecules in animal models of extrinsic allergic asthma offers new possibilities in management of allergic disease.