Abstract
Antiphospholipid antibodies (aPL Abs) are associated with thrombosis in patients with the antiphospholipid syndrome (APS). There is strong evidence that aPL Abs are pathogenic in vivo from studies in animal models. Furthermore, there are now convincing data indicating that activation of complement is involved in those processes. This report addresses current modalities of treatment, as well as recent findings with respect to molecular events triggered by aPL Abs on endothelial cells, platelets, monocytes and complement activation. A separate section addresses recent findings with regard to the putative receptor(s) recognized by aPL Abs on target cells. Based on experimental evidence using in vitro and in vivo models, new targeted therapies for treatment and/or prevention of thrombosis in APS are proposed and discussed.
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