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我的贡献,我的梦想——展望抗磷脂综合征的未来。

My contribution, my dream - a look at the future of APS.

作者信息

Koike T

机构信息

Department of Medicine II, Hokkaido University Graduate School of Medicine, and NTT Sapporo Medical Center, Sapporo, Japan

出版信息

Lupus. 2014 Oct;23(12):1332-4. doi: 10.1177/0961203314534306.

Abstract

We found, in 1994, that the epitope for anticardiolipin antibodies (aCL) developed when β2-glycoprotein I (β2GPI) was adsorbed on polyoxygenated polystyrene plates. We also found, in 2009, that the cleaved form of β2GPI (nicked β2GPI) was bound to angiostatin 4.5 and attenuated its antiangiogenic property. We described in 2000 that antiprothrombin antibodies were bound to prothrombin exposed to immobilized phosphatidylserine (aPS/PT) and more than 95% of antiphospholipid syndrome patients who were positive for aPS/PT had lupus anticoagulant. We demonstrated that in the cells stimulated by human monoclonal anti-β2GPI antibodies, p38 mitogen-activated protein kinase phosphorylation was observed in the presence of β2GPI. Furthermore, we found that complement activation was essential for thrombus formation in patients with the antiphospholipid syndrome in vivo.

摘要

1994年,我们发现当β2-糖蛋白I(β2GPI)吸附在多氧化聚苯乙烯板上时会产生抗心磷脂抗体(aCL)的表位。2009年,我们还发现β2GPI的裂解形式(缺口β2GPI)与血管抑素4.5结合并减弱了其抗血管生成特性。我们在2000年描述了抗凝血酶原抗体与暴露于固定化磷脂酰丝氨酸的凝血酶原(aPS/PT)结合,并且aPS/PT呈阳性的抗磷脂综合征患者中超过95%有狼疮抗凝物。我们证明,在人单克隆抗β2GPI抗体刺激的细胞中,在有β2GPI存在的情况下观察到p38丝裂原活化蛋白激酶磷酸化。此外,我们发现补体激活对于抗磷脂综合征患者体内血栓形成至关重要。

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