Abstract
Antiphospholipid syndrome (APS) is a systemic autoimmune disease, characterized by thrombosis, obstetric complications and the presence of antiphospholipid antibodies (aPL), which drive endothelial injury and thrombophilia. Extracellular vesicles (EVs) have been implicated in endothelial and thrombotic pathologies. Here, we characterized the quantity, cellular origin and the surface expression of biologically active molecules in small EVs (sEVs) isolated from the plasma of thrombotic APS patients (n = 14), aPL-negative patients with idiopathic thrombosis (aPL-neg IT, n = 5) and healthy blood donors (HBD, n = 7). Nanoparticle tracking analysis showed similar sEV sizes (110–170 nm) between the groups, with an increased quantity of sEVs in patients with APS and aPL-neg IT compared to HBD. MACSPlex analysis of 37 different sEV surface markers showed endothelial (CD31), platelet (CD41b and CD42a), leukocyte (CD45), CD8 lymphocyte and APC (HLA-ABC) cell-derived sEVs. Except for CD8, these molecules were comparably expressed in all study groups. sEVs from APS patients were specifically enriched in surface expression of CD62P, suggesting endothelial and platelet activation in APS. Additionally, APS patients exhibited increased CD133/1 expression compared to aPL-neg IT, suggesting endothelial damage in APS patients. These findings demonstrate enhanced shedding, and distinct biological properties of sEVs in thrombotic APS.
Highlights
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thromboses and/or obstetric complications, as confirmed with the presence of antiphospholipid antibodieson at least two occasions, 12 weeks apart [1]
A similar percentage of thrombosis was observed between APS patients and aPL-neg IT patients
The biochemical variables that were measured, showed no significant differences between the groups
Summary
Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thromboses and/or obstetric complications, as confirmed with the presence of antiphospholipid antibodies (aPL)on at least two occasions, 12 weeks apart [1]. Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thromboses and/or obstetric complications, as confirmed with the presence of antiphospholipid antibodies (aPL). Associated clinical manifestations may include livedo reticularis, cutaneous ulcerations, thrombocytopenia, haemolytic anaemia, valvular heart disease and nephropathy, among others [2]. Laboratory criteria for APS include testing for lupus anticoagulant (LA), moderately high titre anti-cardiolipin (aCL) or anti-β2 glycoprotein (anti-β2GPI). The presence of non-criteria antibodies, such as anti-phosphatidylserine/ prothrombin antibodies (aPS/PT), may increase the risk of clinical manifestations of APS [3]. The degree of risk associated with aPL depends on the characteristics of their profile, and on the presence of additional thrombotic risk factors, such as hyperlipidaemia, arterial hypertension, diabetes, smoking, obesity, low grade inflammation and use of contraceptives [1]. Despite some improvements in the diagnosis and prognosis of APS and prevention of thrombosis reoccurrence, robust laboratory biomarkers are still lacking
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