Tissue factor in the antiphospholipid syndrome

Department of Medicine and Thurston Arthritis Research Center, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7280, USA.
Lupus (Impact Factor: 2.2). 02/2008; 17(10):952-8. DOI: 10.1177/0961203308096662
Source: PubMed


Antiphospholipid (aPL) antibodies are clinically important acquired risk factors for thrombosis and pregnancy loss and are thought to have a direct prothrombotic effect in vivo. Data suggest that a major mechanism by which aPL antibodies contribute to thrombophilia is the upregulation of tissue factor (TF) (CD142) on blood cells and vascular endothelium. TF is the physiological trigger of normal blood coagulation and thrombosis in many hypercoagulable conditions. This article reviews the physiology of TF, the molecular regulation of TF expression and the effects of aPL antibodies on intravascular TF regulation and expression. Inhibition of TF and the pathways by which aPL antibodies induce TF expression are potentially attractive therapeutic targets in the antiphospholipid syndrome.

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    • "The interaction of the anti-b 2 GPI/b 2 GPI/PL complex in genetically susceptible individuals disturbs the homeostatic reactions by the activation of the vascular endothelium and platelets [12] [13] [23] [26]. In endothelial cells there is an increased expression of adhesion molecules such as ICAM-1, VCAM-1 and E-selectin [14] [27], in addition to allowing the expression of tissue factor [28] and the production of proinflammatory cytokines such as IL-1b, IL-6, IL-8, TNF-a and MCP-1 perpetuating activation and inducing a prothrombotic state [29] [30]. "
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