抗磷脂抗体综合征(APS)临床表现为反复的动静脉血栓、流产和血小板减少，常继发于系统性红斑狼疮等自身免疫性疾病，该疾病易发血栓的机制目前仍未明确。在我们以往的研究证实抗磷脂抗体可以通过抑制凝血相关因子和激活内皮细胞而促进血栓形成的基础上，我们拟研究在连接感染和血栓起核心作用的天然免疫细胞如中性粒细胞、单核细胞和树突状细胞在Ⅰ型干扰素的活化下参与血栓形成的机制，Ⅰ型干扰素诱导天然免疫细胞表达组织因子的细胞内信号通路,研究APS患者外周血中性粒细胞、单核细胞和DC表面组织因子和蛋白酶激活受体1（PAR1）的表达，并通过所建立的动物模型研究Ⅰ型干扰素单克隆抗体、PAR1受体拮抗剂和DNase1酶对血栓形成的干扰抑制试验，以期发现抑制APS血栓形成的新的治疗方法。为APS的新的治疗策略奠定实验基础。

Antiphospholipid syndrome (APS) is an autoimmune disease charateried by of recurrent arterial,venous thrombosis,abortion and thrombocytopenia. It is usully secondary to systemic lupus erythematousis. The machnism of thrombosis caused by APS is not unclear. Previously,our study indicated that antiphospholipid antibody can bind to and interfered with the function of the co-factors, i.e. thrombin,plasmin and beta2GP1, and induced thombosis of mice model. In this study, we want to investigate if the innate immune cells,i.e.neutrophil,monocyte and DC which is plays an key role in the coagluantion and infection restriction involved in the thrombosis in APS. The cell signal pathway of type1 interferon inducing the expression of tissue factor will also be investigated. By investigating the status of the expression of tissue factor, PAR1, and annimal study to see the effect of anti-interferon α antibody, PAR recepte 1 angonist and DNase1 reducing thrombosis in vivo, we can find a clue to find new method to prevent thrombosis.