*5.1.2 Small extracellular vesicles*

To date, only a study by Stok et al. has investigated the presence of sEVs in plasma of APS patients (**Table 2**). Compared to HBDs, significantly increased levels of sEVs were observed in APS patients. In addition, sEVs from different cellular origin: platelet (CD41b+, CD42a+), lymphocyte (CD8+), leukocyte (CD45+) and endothelial (CD31+) were detected. Flow cytometric characterization of sEVs defined a subpopulation of vesicles that were positive for P-selectin (CD62P) and the endothelial progenitor cell marker (CD133/1). sEVs from APS patients were enriched in surface expression of P-selectin, suggesting endothelial and platelet activation in APS. In addition, APS patients showed increased CD133/1 expression compared to aPL- patients with thrombosis, suggesting endothelial damage in APS [13]. The authors of this study suggest that increased levels of sEVs with distinct biological properties circulate in patients with thrombotic APS.
