Interactions between blood cells and stimulated or injured venule
Leukocytes roll on stimulated endothelium before migrating to sites of inflammation or vascular injury. This initial and essential step is largely mediated by the selectins and their ligands. The leukocyte receptors involved cluster on small membrane projections (microvilli). After activation, leukocytes firmly adhere to endothelial cells as a result of the interaction between their β2 integrins and members of the immunoglobulin superfamily on the endothelium. The same types of receptors also mediate the extravasation of leukocytes. Leukocytes migrate, using their β1 integrins, toward a chemotactic stimulant (in this case produced by bacterial invasion). Vascular injury immediately induces endothelial cells to release the contents of their storage granules (Weibel–Palade bodies), including P-selectin and von Willebrand factor (vWF). Von Willebrand factor is quickly deposited on the exposed extracellular matrix, where it plays a crucial role in the adhesion of platelets to the damaged site. Degranulation of platelets and activation of the platelet integrin αIIbβ3 induce further accumulation of platelets (aggregation) and promote the recruitment of neutrophils and monocytes to participate in repair. The platelet plug is stabilized by strands of fibrin. Platelet rolling, mediated by P-selectin on endothelium or by von Willebrand factor on the extracellular matrix, may represent an initial step in hemostasis, analogous to the rolling of leukocytes in inflammation.
Ref: Frenette, PS, Wagner, DD. Adhesion molecules--Part II: Blood vessels and blood cells. N Engl J Med. 335:43-45. 1996