作者: Jaap-Jan Zwaginga , Paula da Costa Martins
DOI: 10.1160/TH05-10-0705
关键词:
摘要: C irculating platelet-leukocyte aggregates (PLA) were first reported in the early 1960s and long considered as being mere markers for vascular disease which platelet activation occurs (2–6). In this respect, an increase of PLA circulation can be found under clinical conditions such 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 a -granules surface (13–15). The main ligand P-selectin Glycoprotein Ligand-1 (PSGL-1), disulfide-linked homodimer constitutively expressed on most (16–18). Also, integrin-mediated interactions glycoprotein (GP) IIb/IIIa – fibrinogen bridging molecule well s z-integrin CD11b/CD18 (mac-1)or intercellular adhesion molecule- 2 leukocytes, thrombospondin CD36 (GPIV) leukocyte possible. Furthermore, immune complex between Fc? RII (CD32) neutrophil RIIIb, GPIba junctional adhesive molecule-C binding .