Cellular interactions play a key role in diverse biological processes within the cardiovascular system. Targeting of leukocytes to sites of inflammation is viewed as a multistage process of sequential involvement of distinct adhesion molecules on the leukocyte and endothelial cell (EC) surface that is dictated by the local fluid dynamic environment. For neutrophils, the initial contact and rolling along the vessel wall are mediated primarily by selectins. Subsequent firm adhesion requires activation of neutrophil β₂ integrins and binding to their ligand ICAM-1 on the EC surface. The final step of this cascade of events includes neutrophil transmigration to extravascular tissue space. The neutrophil model of emigration in inflammation has been extended and refined to account for monocyte and T cell interactions with ECs. Platelet adhesion to thrombogenic surfaces (i.e. immobilized von Willebrand factor) under flow follows the general principles of leukocyte extravasation. More specifically, platelet glycoprotein (GP) Ibα appears to mediate an initial selectin-like tethering platelet–vWf interaction, followed by α_IIββ₃ integrin activation and firm adhesion. Some of the signaling mechanisms associated with cellular interactions in inflammatory and thrombotic processes are discussed. These basic principles are also discussed in the context of tissue engineering research.