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An Update on Pathogenic Mechanisms Mediated by Antiphospholipid Antibodies

Ellis Doan, MD1, Neha Dang, MD1, and Silvia S Pierangeli, PhD1,2

Antiphospholipid (aPL) antibodies are associated with thrombosis and are a risk factor for recurrent pregnancy loss and obstetric complications in patients with the antiphospholipid syndrome (APS). It is generally accepted that the major autoantigen for aPL antibodies is β2glycoprotein I (β2GPI), which mediates the binding of aPL antibodies to target cells (i.e. endothelial cells [EC], monocytes, platelets, and trophoblasts) leading to thrombosis and fetal loss. This review article addresses molecular events triggered by aPL antibodies on EC, platelets, and monocytes, and its effect on complement activation. Current knowledge with regard to the putative receptor(s) recognized by aPL antibodies on target cells, as well as novel mechanisms that involve fibrinolytic processes, are also reviewed. A section is devoted to the description of thrombotic and inflammatory processes that lead to obstetric complications mediated by aPL antibodies. Based on experimental evidence using in vitro and in vivo models, new targeted therapies for treatment and/or prevention of thrombosis and pregnancy loss in APS are proposed.Int J Adv Rheumatol 2010;8(1):16–26.

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