Arrest chemokines, such as CXCL2, CXCL8, and CCL5 (alone or as heterodimer with CXCL4) bind to the glycosaminoglycans on the surface of endothelial cells, immobilize, and mediate firm adhesion of rolling monocytes.
Leukocyte integrins and their ligands on endothelial cells, including intercellular adhesion molecules (ICAMs), then mediate firm leukocyte adhesion [ 20].
Separately, sLeX/P-selectin interactions support rolling and aICAM-1/ICAM-1 interactions mediate firm adhesion.
After injury ICAM-1 interacts with leukocyte integrins to mediate firm adhesion of activated neutrophils to endothelium and diapedesis [ 4– 7].
Endothelial ICAM-1 mediates firm arrest of rolling monocytes by binding to integrins LFA-1 and Mac-1 [45].
The αMβ2 (Mac-1) integrin mediates firm adhesion of leukocytes to inflamed vessels by interacting with its endothelial cell counter-receptor intercellular adhesion molecule-1.
Intercellular adhesion molecule-1 (ICAM-1), a cell surface molecule of the immunoglobulin superfamily, mediates firm adhesion of circulating neutrophils and thereby enhances their transmigration through the endothelial barrier.
The extracellular region of ICAM binds ligands including fibrin, certain pathogens, and integrins of activated leukocytes, mediating their firm adhesion to endothelial cells.
Activated integrins, in particular β1, β2 and β3 integrins, mediate a firm adhesion to endothelial cells by binding their ligands such as ICAM, VCAM, PECAM or other integrins [ 4- 6] leading to transendothelial migration.
Respectively, these well-characterized proteins mediate the firm adhesion of leukocytes to endothelial cells as well as hepatocytes and the chemotaxis of monocytes/macrophages.
