Conclusion
Platelets are a potential target for circulating aPL that may cause antibody mediated thrombosis. In vitro studies performed in the aggregometer or in flowing conditions and the evaluation of platelet activation markers in vitro and in vivo in patients with the APS demonstrated the ability of aPL to interact with platelets and promote their function. The most reliable explanation for the prothrombotic action of aPL in platelets includes, first, previous platelet activation and the binding of them to platelet membrane phospholipid bound proteins, mainly β2-glycoprotein I. Then, in a second step, aPL may act activating platelets, via FcγRIIA or complement C5-9 formation. However, several points of this suggested mechanism of action of aPL on thrombus formation are not clearly established and further studies on the interaction between platelet and aPL are needed.
Keywords
- Systemic Lupus Erythematosus
- Platelet Activation
- Lupus Anticoagulant
- Anticardiolipin Antibody
- Platelet Membrane
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Reverter, JC., Tàssies, D. (2006). Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets. In: Khamashta, M.A. (eds) Hughes Syndrome. Springer, London. https://doi.org/10.1007/1-84628-009-5_32
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