Integrin‐mediated adhesion to the vascular endothelium is an essential step in leukocyte diapedesis. We show that the chemokines 10‐kDa inflammatory protein (IP10) and monokine induced by IFN (Mig) induce rapid and transient adhesion of human IL‐2‐stimulated T lymphocytes (IL‐2 T cells) to immobilized integrin ligands through their receptor CXCR3, which is selectively expressed on activated T cells. Induction of adhesion by IP10 and Mig was already observed at subnanomolar concentrations and was maximal at 5 – 10 nM, resulting in three‐ to sixfold increase in adhesion of IL‐2 T cells over background. No effect was seen with resting naive/memory T cells which lack CXCR3 and migration responses to IP10 and Mig. Both chemokines are produced in human umbilical vein endothelial cells (HUVEC) upon stimulation with IFN‐γ and TNF‐α. These chemokines induce IL‐2 T cell adhesion also when captured on the surface of endothelial cells. Under conditions of flow, IL‐2 T cells roll and rapidly adhere to IP10/Mig‐expressing HUVEC, and anti‐CXCR3 mAb treatment reduces arrest and firm adhesion. This is the first study that shows chemokine‐induced adhesion in activated memory/effector T cells which represent the fraction of T cells that are selectively mobilized in inflammation. The critical role of IFN‐γ as inducer of IP10/Mig production in HUVEC indicates that these chemokines are essential mediators of effector T cell recruitment to IFN‐γ‐dependent pathologies.