免疫性血小板减少症(ITP)是一种由于自身免疫异常所致的血小板生成、破坏加速的出血性疾病。我们前期研究了巨核细胞对ITP反向免疫调控的机制。期间我们建立了巨核细胞分离富集培养的平台，并通过表达谱芯片发现巨核细胞表达粘附分子的异常。由此我们推断ITP患者的骨髓微环境可能影响巨核细胞的定位和分化发育过程，进而对ITP的自身免疫存在影响。我们拟通过本课题研究ITP患者骨髓巨核细胞的定位以及与骨髓微环境的关系，并通过过表达和沉默PECAM-1和SDF-1和CD11a明确其对巨核细胞成熟分化的影响。并进一步分析其对自身免疫的影响。最后通过ITP 主动型小鼠模型，体内研究对ITP 小鼠模型骨髓巨核细胞定位、分化成熟及对ITP自身免疫的影响及其机制。本研究将明确ITP患者骨髓微环境对巨核细胞及ITP自身免疫的影响，进一步明确ITP的发病机制,并为发展新的治疗措施提供理论基础。

Immune thrombocytopenia (ITP) is a kind of platelet production, due to autoimmune destruction caused by accelerated hemorrhagic disease. We studied the mechanism of megakaryocyte in reverse immune regulation in ITP. We established a platform of megakaryocytes enrichment separation, and found abnormal megakaryocyte expression of adhesion molecules. We speculated that ITP patients with bone marrow microenvironment may affect megakaryocyte differentiation and localization process and influence the autoimmunity of ITP. We intend this topic by positioning the relationship of ITP in bone marrow megakaryocytes and bone marrow microenvironment, and through over expression and silencing of PECAM-1 and SDF-1 and CD11a identify the effects on megakaryocyte differentiation. And further analysis of its impact on immune. Finally through the ITP active mouse model, studies on the effects of ITP mouse model of bone marrow megakaryocyte differentiation and maturation, localization of ITP and autoimmunity and its mechanism. This study will clearly affect patient’s bone marrow microenvironment of ITP on megakaryocyte and ITP antibodies, to further clarify the pathogenesis of ITP, and provide a theoretical basis for the development of new therapeutic measures.