抗磷脂综合征（APS）临床表现为反复的动静脉血栓和流产，目前有关非抗体所介导的血栓形成机制是APS研究的热点，我们前期研究表明原发性APS也存在Ⅰ型干扰素通路的异常活化，且诱导生长停滞特异性基因6（GAS6）和其配体AXL蛋白的表达增加。基于磷脂酰丝氨酸是GAS6激活血小板和内皮细胞的过程中的必要的成员，我们提出了I型干扰素诱导的GAS6/AXL通路的活化参与或与抗磷脂抗体（抗磷脂酰丝氨酸抗体）协同参与血栓形成新的机制。本研究拟通过体外实验研究GAS6/磷脂酰丝氨酸/抗磷脂酰丝氨酸抗体三者在血管内皮细胞/血小板活化和产生组织因子和粘附分子的影响，并用野生型和GAS6-/-敲除鼠研究GAS6和抗磷脂酰丝氨酸抗体协同促进血栓的机制。通过以上研究可对APS的血栓形成机制有新的认识，并为APS新的治疗策略奠定实验基础。

Antiphospholipid syndrome (APS) is a multi-systemic autoimmune disorder characterized by vascular thrombosis and/or pregnancy morbidity. The current research focused on the pathogenesis of non-autoantibody-mediated thrombosis. Our previous studies have showed the abnormal of Type I interferon pathway associated with primary APS via inducing the expression of growth arrest-specific gene 6 (GAS6) and its ligand AXL protein. As phosphatidylserine is one of the essential issues of GAS6-induced platelets and endothelial cells activation, we proposed that type I interferon-induced GAS6/AXL pathway activation is involved or synergistic with the anti-phosphatidylserine (aPL) in the pathogenesis of thrombosis in APS. In the current study, we investigated the effects of GAS6/phosphatidylserine/ anti-phosphatidylserine antibodies on the activation of vascular endothelial cells/platelets and the production of tissue factor and adhesion molecules in vitro. Besides, using GAS6-/- knockout mice, we discussed the mechanism of GAS6 and anti-phosphatidylserine antibodies synergistically promote thrombosis in APS model. Through all the above studies, we could gain a new insight into the thrombosis pathogenesis of APS, and might elucidate the mechanism of type I interferon-induced GAS6 / AXL pathway invovled or synergistic with aPL (anti-phosphatidylserine antibody) in the development of thrombosis in APS, which might be the experiment foundation for the treatment strategy.