特发性血小板减少性紫癜共刺激分子表达的研究进展

特发性血小板减少性紫癜（ITP）是一种自身免疫性疾病，其发病机制尚未完全明确，目前已证实，ITP患者体内存在T、B淋巴细胞的异常活化和B淋巴细胞依赖Th细胞辅助而产生自身抗血小板抗体。在T、B淋巴细胞相互作用和产生自身抗体的病理过程中，CD80、CD86与其配体CD28、CTLA4结合及CD40与其配体CD40L相互作用提供的共刺激信号起了重要的作用。研究表明共刺激分子过度表达有可能激活自身反应性T淋巴细胞，导致自身免疫病的发生。

Recent studies on the expression of costimulatory molecules in idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura(ITP)is autoimmune disease,now its pathogenesis is still unclear.In recent years,numerous studies have shown that T cells and B cells are activated abnormally and under the aiding of helper T cells(Th),B cells produce antiplatelet autoantibody in ITP patients.The key role of costimulatory molecules is necessary in the interaction of T cells and B cells and in the pathological process of producing autoantibody.The interactions between CD80 /CD86-binding ligand CD28 or CTLA-4 and CD40-CD40 ligand supply costimulatory signals,which may play an important role in the stimulation of immune system in ITP.Increasing evidences indicate that when ITP occurred,overexpressed costimulatory molecules maybe activate autoreactivity T cells and cause autoimmune disease.Researching progress of expression of costimulatory molecules will be summurized in this paper.