الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Platelets play a complex role in hemostasis and thrombosis. The expression of multiple membrane receptors, both constitutive and activation-dependent, mediates platelet adhesion and aggregation at sites of vascular lesion. Platelets normally circulate in a quiescent state, their activation leads to exocytosis of granular constituents, release of newly synthesized mediators, change their shape as well as the expression pattern of adhesive molecules. Many of the same mechanisms that play a role in hemostasis and thrombosis facilitate platelet participation in other physiological or pathological processes including inflammation, malignancy, heparin-induced thrombocytopenia and the immune response. Platelet receptors such as GPIb/IX/V, P-selectin, P-selectin glycoprotein ligand 1, CD40 and the αIIbß3 integrin, crucial to hemostasis, have been implicated in the progression of such inflammatory conditions as atherosclerosis, rheumatoid arthritis and inflammatory bowel disease, in the progression and metastatic spread of malignancies, and in the immune response to bacterial challenge. The release of platelet granular contents, including adhesive proteins, growth factors and chemokines/cytokines, that serve to facilitate hemostasis and wound repair, also function in acute and chronic inflammatory disease and in tumor cell activation and growth. Platelets contribute to host defence as they recognise bacteria, recruit traditional immune cells to the site of infection and secrete bactericidal mediators. They also have been implicated in the development of alloantibody-mediated transplant rejection. Alloantibodies appear to recruit and activate platelets via platelet Fc receptors. In addition, alloantibodies can activate complement, which then causes damage to the endothelium, with the corresponding recruitment of platelets.