The interaction between aPL (particularly anti-β2GPI antibodies) and endothelium does represent a potential pathogenetic mechanism for the thrombotic manifestations of the syndrome. The autoantibody-mediated EC activation probably plays a role in sustaining the appearance of a proadhesive, proinflammatory, and procoagulant phenotype. The heterogeneity of the APS clinical manifestations is likely linked to the varied effects that aPL can induce on ECs and to the different functions that ECs display depending on the anatomic localization.
|Number of pages||16|
|Journal||Rheumatic Disease Clinics of North America|
|Publication status||Published - 2001|
ASJC Scopus subject areas