The recruitment of leukocytes from the blood is one of the most dramatic cellular responses to tissue damage and inflammation, and is central to the physiologic trafficking of lymphocytes. Leukocyte extravasation is exquisitely regulated in vivo by mechanisms of selective leukocyteendothelial cell (EC) recognition, which can display extraordinaryspecificityin relation to the inflammatorystimulus, the stage of the inflammatory response, and the tissue site or organ involved. Examples include the almost exclusive attachment of eosinophils to venules in allergic reactions, the specific recruitment of neutrophils early in acute inflammation, and the tissue-selective interaction of lymphocyte subsets with high endothelial venules (HEVs) in organized lymphoid tissues.

Adhesion receptors (ARs) mediate and help direct leukocyte-EC interactions (Figure 1; reviewed in Springer, 1990; Pober and Cotran, 1990; Berg et al., 1991). Paradoxically, however, individual receptors often participate in multiple leukocyte-EC interactions that are quite independently regulated in vivo. For example, the vascular E-selectin (ELAM-1) binds both neutrophils and skin-homing memory T cells, yet is thought to support selective recruitment of neutrophils during acute inflammation and of cutaneous memory T cells during chronic inflammation in the skin (Picker et al., 1991a, and references therein). Such observations cannot be explained by simple lockand-key models of cell-cell recognition, and seem to require a more complex control of leukocyte-EC interactions in vivo.