Endothelial activation is an integral component of inflammatory rheumatic diseases, and also of atherosclerosis. Leukocytes emigrate from the blood into inflamed tissues through a series of adhesion events (“the adhesion cascade”), each of which is dependent upon the state of endothelial cell activation. Initial rolling of neutrophils on vascular endothelium is mediated by transient interactions between selectins (L-selectin on leukocytes, E-selectin on cytokine-activated endothelial cells (EC) and P-selectin on both activated EC and activated platelets) and carbohydrate-bearing counter-structures on the opposing cell. Whilst rolling, leukocytes become exposed to activating signals (such as chemokines), resulting in an upregulation of the capacity of b2 integrins (eg LFA-1, Mac-1) to bind ligands (eg ICAM-1, -2) on EC. This integrin-mediated secondary adhesion results in leukocyte arrest and is followed by their transmigration into the tissues. In the case of mononuclear cells, adhesion of a4 integrins to EC ligands (eg VCAM-1) may contribute to both the rolling and firm adhesion stages of their interaction with EC. The talk will focus on comparisons between inflammatory rheumatic diseases and atherosclerosis, and will discuss recent technical advances that have allowed an improved understanding of the patterns of endothelial activation and adhesion molecule expression that occur in acute and chronic inflammatory settings.
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