Chefarzt Institut für Labormedizin (IFLM), Solothurner Spitäler AG, Kantonsspital Olten, Baslerstrasse 150, 4601, Olten, Switzerland.
Curr Rheumatol Rep. 2010 Feb;12(1):58-63. doi: 10.1007/s11926-009-0079-0.
The antiphospholipid syndrome (APS) is an autoimmune disease characterized by thrombosis, recurrent fetal loss, and the presence of antiphospholipid antibodies (aPL). Recent data support the idea that the thrombotic activity in APS patients is attributed to enhanced cytokine release via activation of certain Toll-like receptors. To investigate these mechanisms more precisely, different experimental approaches were used to investigate this connection in detail. IgG fractions and/or monoclonal aPL, either generated from murine or human B cells were intensely used for stimulation experiments of monocytes, endothelial cells, or dendritic cells. All these stimuli induced an enhanced expression and secretion of cytokines, especially tumor necrosis factor (TNF)-alpha, caused by specific regulation or activation of Toll-like receptors. Using specific agonists or inhibitors could confirm the causal connection of these stimulatory effects. This review focuses on these recent developments, connecting the binding of aPL with the activity of Toll-like receptors, especially in monocytes, endothelial cells, and dendritic cells.
抗磷脂综合征（APS）是一种自身免疫性疾病，其特征是血栓形成、复发性胎儿丢失和抗磷脂抗体（aPL）的存在。最近的数据支持这样一种观点，即 APS 患者的血栓形成活性归因于通过激活某些 Toll 样受体导致细胞因子释放增加。为了更精确地研究这些机制，使用了不同的实验方法来详细研究这种联系。IgG 片段和/或单克隆 aPL，无论是从鼠源还是人源 B 细胞产生的，都被强烈用于刺激单核细胞、内皮细胞或树突状细胞的实验。所有这些刺激物通过 Toll 样受体的特异性调节或激活诱导细胞因子（尤其是肿瘤坏死因子（TNF）-α）的表达和分泌增加。使用特异性激动剂或抑制剂可以证实这些刺激作用的因果关系。这篇综述重点介绍了这些最新的发展，将 aPL 的结合与 Toll 样受体的活性联系起来，特别是在单核细胞、内皮细胞和树突状细胞中。
