Although our understanding of the pathogenesis of the chief forms of inflammatory bowel disease, Crohn's disease, and ulcerative colitis remains incomplete, progress is being made in identifying essential components.¹ The presence of large numbers of varied leukocytes within affected tissue where they are normally sparse makes it axiomatic that active disease is dependent on the recruitment of these cell populations. Recruitment is now known to proceed through a stereotypical series of steps that depend on selective adhesion molecules (SAMs). These include cell-surface integrins, heterodimers formed by various combinations of α and β subunits. Integrins with an α₄ chain appear . . .