Abstract
Antiphospholipid antibodies (aPL), particularly those directed against β2-glycoprotein I, cause activation of vascular cells (endothelial cells, platelets,
monocytes) and release of extracellular vesicles (EVs), which include exosomes and
microparticles (MPs). MPs, particularly endothelial MPs, have been most extensively
studied in antiphospholipid syndrome (APS). Compared with healthy controls, patients
with aPL have significantly higher levels of circulating endothelial and platelet
MPs, including MPs expressing immunological and functional tissue factor. Although
a consistent relationship of EVs with APS-related thrombosis and obstetric events
has not yet been demonstrated, elevated levels of MPs occurring remote from thrombotic
events suggest a chronic state of vascular activation in APS. In addition to being
a marker of cellular activation, EVs express bioactive lipids, proteins, and nucleic
acids, particularly microribonucleic acid (microRNA). EVs may potentially play a pathogenic
role in APS by stimulating thrombosis through tissue factor-dependent and independent
mechanisms and by promoting vascular activation. Further research is needed to understand
these mechanisms and to determine whether EVs may be a useful biomarker to identify
patients with aPL at highest risk of clinical events.
Keywords
antiphospholipid syndrome - antiphospholipid antibodies - microparticles - thrombosis
- endothelial cells - platelets
