Pathophysiological Mechanisms in the Antiphospholipid Syndrome: B2GPI Regulation of FXI-FXIa

抗磷脂综合征的病理生理机制：B2GPI 对 FXI-FXIa 的调节

• 批准号: nhmrc : 510130
• 负责人: Prof Steven Krilis
• 金额: $ 35.38万
• 依托单位: The University of New South Wales
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2008
• 资助国家: 澳大利亚
• 起止时间: 2008-01-01 至 2010-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/pathophysiological-mechanisms-antiphospholipid-fxi-fxia/94379
• 关键词: Pathophysiological; Mechanisms; Antiphospholipid; Syndrome; B2GPI

The major protein that the antibodies in the antiphospholipid syndrome (APS) bind is called Beta 2-GPI. Antibodies to Beta 2-GPI are associated with recurrent miscarriage, intrauterine growth retardation, clots and stroke. Treatment of patients with the APS are treated with medication that has significant side effects. The development of more targeted and effective therapies for the APS requires a greater understanding of how the antibodies cause their effects, which is addressed in this study.

抗磷脂综合征（APS）中抗体结合的主要蛋白质称为β 2-GPI。β 2-GPI抗体与复发性流产、宫内发育迟缓、血栓和中风有关。APS患者的治疗采用具有显著副作用的药物治疗。为APS开发更有针对性和更有效的治疗方法需要更好地了解抗体如何引起其作用，这在本研究中得到了解决。