Association between extracellular vesicles (EVs) and thrombosis in antiphospholipid syndrome.

Abstract

BackgroundAntiphospholipid syndrome (APS) is characterized by thrombosis or pregnancy complications associated with the presence of antiphospholipid antibodies (aPLs). Although the exact mechanisms are unclear, aPLs can increase the expression of tissue factor on platelets, leukocytes, and endothelial cells, leading to hypercoagulability. Extracellular vesicles (EVs) can also be released during this process and play a key role in immune regulation and thrombosis related to APS.AimsTo evaluate the association between circulating levels of EVs and thrombosis related to APS, as well as inflammatory markers.MethodsCase-control study including patients with thrombotic APS (t-APS) and healthy controls (HC). EVs expressing the following antigens were quantified by flow cytometry: CD41 (platelet integrin alpha IIb), CD162 (P-selectin glycoprotein ligand 1), CD31 (platelet and endothelial cell adhesion molecule 1), CD142 (tissue factor), and CD62 (P-selectin). EV levels were compared between groups and correlated with APS clinical and inflammatory parameters.ResultsA total of 69 t-APS patients and 46 HC were included. CD162+EV, CD31+EV, and CD41+EV levels were higher in t-APS patients compared to controls. CD41+EV levels were associated with venous thrombosis (p = .04) and multiple thrombosis (p = .07). Levels of CD162+EV, CD31+EV, CD142+EV and CD62P + EV were positively correlated with levels of interleukin-1 beta (IL-1β).ConclusionEVs expressing antigens related to platelet and endothelial cell activation and adhesion, as well as platelet-leukocyte interaction, were associated with thrombosis related to APS. The correlation between EV levels and IL-1β levels further underscore the association between EV release and thromboinflammatory responses in APS. Our results demonstrate the involvement of EVs in the interaction between inflammation and thrombosis in APS.