Meroni P L, Raschi E, Testoni C, Tincani A, Balestrieri G
Allergy and Clinical Immunology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Milan, Italy.
Rheum Dis Clin North Am. 2001 Aug;27(3):587-602. doi: 10.1016/s0889-857x(05)70222-2.
The interaction between aPL (particularly anti-beta 2GPI antibodies) and endothelium does represent a potential pathogenetic mechanism for the thrombotic manifestations of the syndrome. The autoantibody-mediated EC activation probably plays a role in sustaining the appearance of a proadhesive, proinflammatory, and procoagulant phenotype. The heterogeneity of the APS clinical manifestations is likely linked to the varied effects that aPL can induce on ECs and to the different functions that ECs display depending on the anatomic localization.
抗磷脂抗体（尤其是抗β2糖蛋白I抗体）与内皮细胞之间的相互作用确实代表了该综合征血栓形成表现的一种潜在发病机制。自身抗体介导的内皮细胞活化可能在维持促黏附、促炎和促凝血表型的出现中起作用。抗磷脂综合征临床表现的异质性可能与抗磷脂抗体对内皮细胞可诱导的多种效应以及内皮细胞根据解剖定位所显示的不同功能有关。
