Meroni Pier Luigi, Raschi Elena, Testoni Cinzia
Allergy and Clinical Immunology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Via L. Ariosto 13, 20145 Milan, Italy.
Autoimmun Rev. 2002 Feb;1(1-2):55-60. doi: 10.1016/s1568-9972(01)00014-3.
Endothelium activation seems to represent one of the pathogenic mechanisms that induce the trombophilic state of the anti-phospholipid syndrome. The rationale behind such a statement lies on the demonstration that: (a) the major antigen of the anti-phospholipid antibodies (beta 2 glycoprotein I) can be expressed on the endothelial cell membrane, (b) the endothelial beta 2 glycoprotein I offers suitable epitopes for circulating antibodies, (c) the binding of anti-beta 2 glycoprotein I antibodies is capable to induce the appearance of a pro-coagulant and pro-inflammatory phenotype. Both in vitro and in vivo experimental models support such a hypothesis. Although a classical vasculitic process cannot be found in the anti-phospholipid syndrome there is indirect evidence that endothelial activation/damage does occur also in vivo. The demonstration that hydroxymethylglutaryl Co-enzyme A reductase enzyme inhibitors (statins) can block endothelial cell activation induced by anti-beta 2 glycoprotein I antibodies as well as by pro-inflammatory cytokines offers new therapeutical approaches.
内皮细胞激活似乎是诱导抗磷脂综合征血栓形成倾向状态的致病机制之一。这一说法背后的基本原理基于以下证据：(a) 抗磷脂抗体的主要抗原（β2糖蛋白I）可在内皮细胞膜上表达，(b) 内皮细胞β2糖蛋白I为循环抗体提供了合适的表位，(c) 抗β2糖蛋白I抗体的结合能够诱导促凝和促炎表型的出现。体外和体内实验模型均支持这一假说。虽然在抗磷脂综合征中未发现典型的血管炎过程，但有间接证据表明体内也会发生内皮细胞激活/损伤。羟甲基戊二酰辅酶A还原酶抑制剂（他汀类药物）能够阻断抗β2糖蛋白I抗体以及促炎细胞因子诱导的内皮细胞激活，这一发现提供了新的治疗方法。
