Antiphospholipid antibodies and platelets.
The most distinguishing serologic feature of antiphospholipid syndrome (APS) is the moderate to high blood titers of antiphospholipid-binding antibodies (aPL). The pathogenic mechanisms of APS are poorly understood, but may occur as a result of the interaction between anticardiolipin antibodies (aCL), beta-2 glycoprotein-I (beta(2)GP-I) (the aCL cofactor) and blood platelets. However, the relationship between aCL/beta(2)GP-I complexes and platelet aggregation has yet to be clearly elucidated. This article will briefly review aPL, beta(2)GP-I and platelet physiology with respect to recent hypotheses relating aCL/beta(2)GP-I complexes and platelets.
De Jong
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Departments of Internal Medicine and Dermatology, School of Medicine, University of California, Davis, CA 95616, USA.
Ziboh
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Robbins
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D017153:Antibodies, Anticardiolipin / Q000097:blood; D017152:Antibodies, Antiphospholipid / Q000097:blood* / Q000276:immunology; D016736:Antiphospholipid Syndrome / Q000276:immunology*; D001792:Blood Platelets / Q000502:physiology*; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D015539:Platelet Activation / Q000502:physiology; D015398:Signal Transduction; D013929:Thromboxane B2 / Q000096:biosynthesis; D053482:beta 2-Glycoprotein I
D017153:Antibodies, Anticardiolipin; D017152:Antibodies, Antiphospholipid; D006023:Glycoproteins; D016682:Lupus Coagulation Inhibitor; D053482:beta 2-Glycoprotein I; D013929:Thromboxane B2