Semin Thromb Hemost
DOI: 10.1055/s-0037-1599081
Review Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA

Extracellular Vesicles in the Antiphospholipid Syndrome

Shruti Chaturvedi1, Ravi Alluri2, Keith R. McCrae2, 3
  • 1Division of Hematology and Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee
  • 2Department of Cellular and Molecular Medicine, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio
  • 3Department of Hematologic Oncology and Blood Disorders, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio
Further Information

Publication History

Publication Date:
05 May 2017 (eFirst)


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.