Antiphospholipid syndrome (APS) is an autoimmune disease that can occur either as a primary condition (Primary APS) or co-morbidity of an underlying disease. APS is characterized by thrombosis and/or pregnancy complications in the presence of antiphospholipid antibodies (aPLs).

The development of APS thrombotic manifestations is significantly associated with endothelial dysfunction (ED). However, whether ED is a direct consequence of the aPL binding to endothelium or represents a host susceptibility factor is not known.

Through the application of in vitro assays based on patient-derived ECFCs, this project aims to: characterize aPL-mediated ED in APS patients; investigate the presence of aPL-independent ED; identify the molecular pathways responsible for ED in APS patients.