Blank M, Asherson R A, Cervera R, Shoenfeld Y
Department of Medicine B and Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, and Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
J Clin Immunol. 2004 Jan;24(1):12-23. doi: 10.1023/B:JOCI.0000018058.28764.ce.
Antiphospholipid syndrome (APS) is characterized by the presence of pathogenic autoantibodies against beta 2-glycoprotein-I (beta 2GPI). The factors causing production of anti-beta 2GPI remain unidentified, but an association with infectious agents has been reported. Studies on experimental APS models proved that molecular mimicry between beta 2GPI-related synthetic peptides and structures within bacteria, viruses, tetanus toxoid, and CMV are a cause for experimental APS. Any explanation of how microbial infections might set off APS must take into account the observation that all individuals appear to harbor potentially autoreactive lymphocytes, as well as natural antiphospholipid antibodies, but that these cells or antibodies remain innocuous unless somehow activated. Herein, we discuss the association of antiphospholipid antibodies in the infectious state, molecular mimicry as a proposed cause for development of APS, and the contribution of the database to this topic.
抗磷脂综合征(APS)的特征是存在针对β2糖蛋白I(β2GPI)的致病性自身抗体。导致抗β2GPI产生的因素尚不清楚,但已有报道称其与感染因子有关。对实验性APS模型的研究证明,β2GPI相关合成肽与细菌、病毒、破伤风类毒素和巨细胞病毒内结构之间的分子模拟是实验性APS的一个原因。关于微生物感染如何引发APS的任何解释都必须考虑到这样一个观察结果,即所有个体似乎都携带着潜在的自身反应性淋巴细胞以及天然抗磷脂抗体,但这些细胞或抗体除非以某种方式被激活,否则仍然无害。在此,我们讨论感染状态下抗磷脂抗体的关联、作为APS发病原因的分子模拟以及数据库对该主题的贡献。