Thesis (M.Sc.) - Cairo University - Faculty of Medicine - Department of Clinical and Chemical Pathology

Background: Immune thrombocytopenia (ITP), also known as idiopathic thrombocytopenic purpura is an acquired autoimmune disorder, characterized by the production of platelet antibodies, resulting in the destruction of platelets and inhibition of their production. Most reports show that these antiplatelet antibodies induce early destruction of platelets by targeting platelets through Fc receptors in the activated reticuloendothelial system, other studies show that they can act by hypothesis of thrombocytopenia resulting from Fc-independent mechanisms via activation of apoptotic signals. These studies also demonstrated that antiplatelet antibodies including thrombocytopenia are associated with increased apoptotic markers of platelet including annexin v. CXCR4, a chemokine receptor for stromal cell-derived factor(SDF-1) is present on the surface of megakaryocytic lineage as well as on the platelet membrane, and the CXCR4/SDF-1 axis plays an important role in polyploidization and transendothelial migration of megakaryocytes favoring platelet production,this CXCR4/SDF-1 interaction triggers many intracellular signals,such as Akt activation which contributes to apoptotic resistance. Recently, decreased CXCR4 expression on platelet surface had been described in patients with essential thrombocytosis, characterized by megakaryocytic hyperplasia and persistent thrombocytosis. Given that studies focused on examining the circumstance of platelets in ITP are limited

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