Figure 1.

General mechanisms that regulate leukocyte (L)–endothelial interactions. A: An increase in cell number will increase the probability of binding via the laws of mass action. B: Platelet (P) bridging and chemokine secretion by the endothelium to recruit leukocytes. Circulating platelets can adhere to the activated endothelium and either release chemokines that will recruit leukocytes to the cell or physically form a bridge and capture circulating leukocytes. Furthermore, damaged endothelial cells (ECs) can release chemokines to recruit leukocytes, and leukocytes crawling along the endothelium can also release chemokines that will recruit more leukocytes.⁵⁵C: Receptor density. During inflammation, either leukocyte or endothelial ligands on the cell surface that facilitate binding may increase. D: Potential mechanisms that regulate affinity and avidity for binding between adhesion molecules. These include post-translational modifications, change in receptor confirmation, localization on the cell surface, and/or binding and clustering with other surface, cytosolic, or matrix proteins.