Abstract
C irculating platelet-leukocyte aggregates (PLA) were first reported in the early 1960s and long considered as being mere markers for vascular disease in which platelet activation occurs (2–6). In this respect, an increase of PLA in the circulation can be found under clinical conditions such as diabetes, hypertension, congestive heart failure, stroke or acute coronary syndromes (10–12). Platelets are known to bind leukocytes via their P-selectin, which, upon cell activation, is translocated from the a -granules to the cell surface (13–15). The main ligand for P-selectin is P-selectin Glycoprotein Ligand-1 (PSGL-1), a disulfide-linked homodimer constitutively expressed on most leukocytes (16–18). Also, integrin-mediated interactions via platelet glycoprotein (GP) IIb/IIIa – fibrinogen as bridging molecule as well as s z-integrin CD11b/CD18 (mac-1)or intercellular adhesion molecule- 2 on leukocytes, or via thrombospondin – platelet CD36 (GPIV) and leukocyte CD36 are possible. Furthermore, immune complex interactions between platelet Fc? RII (CD32) and neutrophil Fc? RIIIb, as well as platelet GPIba and junctional adhesive molecule-C binding to leukocyte . . . .
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