McFarland J
Platelet and Antibody laboratory, Blood Center of Southeastern Wisconsin, Milwaukee, 53201-2178, USA.
Blood Rev. 2002 Mar;16(1):1-2. doi: 10.1054/blre.2001.0169.
The mechanism of platelet destruction in immune (idiopathic) thrombocytopenic purpura (ITP) is thought to involve production of autoantibody to platelet surface antigens. Once coated with antibody, circulating platelets undergo sequestration via interaction with Fc receptors of macrophages in the reticuloendothelial system. A number of questions remain about the mechanism of platelet destruction in this disease: 1) What is the nature of the stimulus to the immune system that generates antiplatelet antibodies? 2) What is the role of interactions between T-helper lymphocytes and antigen-presenting cells in ITP? 3) What role, if any, is played by the targeting of single or multiple platelet surface glycoproteins by the autoimmune response? 4) Is the site of platelet destruction, intravascular or extravascular, or the state of activation of platelets important in the destruction of platelets?
免疫性（特发性）血小板减少性紫癜（ITP）中血小板破坏的机制被认为涉及针对血小板表面抗原产生自身抗体。一旦被抗体包被，循环中的血小板通过与网状内皮系统中巨噬细胞的Fc受体相互作用而被隔离。关于这种疾病中血小板破坏的机制仍有许多问题：1）产生抗血小板抗体的免疫系统刺激的本质是什么？2）T辅助淋巴细胞与抗原呈递细胞之间的相互作用在ITP中起什么作用？3）自身免疫反应针对单个或多个血小板表面糖蛋白的靶向作用（如果有的话）是什么？4）血小板破坏的部位（血管内或血管外）或血小板的活化状态在血小板破坏中是否重要？
