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.