The Journey of Antiphospholipid Antibodies From Cellular Activation to Antiphospholipid Syndrome

Rohan Willis, E. B. Gonzalez, A. R. Brasier

Research output: Contribution to journalReview articlepeer-review

17 Scopus citations


Pathogenic antiphospholipid antibodies (aPL) are the driving factors of recurrent pregnancy loss and thrombosis that characterize antiphospholipid syndrome (APS). Current evidence indicates that aPL induce a procoagulant phenotype in the vasculature and abnormal cellular proliferation and differentiation in placental tissues to cause the typical clinical features; however, the molecular mechanisms underlying these processes remain incompletely understood. Inflammation serves as a necessary link between the observed procoagulant phenotype and actual thrombus development and is an important mediator of the placental injury in APS patients. However, the underlying mechanisms for these events have also not been fully elucidated. In this review, we will outline the available data that give us our current understanding of the pathophysiology of APS, especially as it relates to the development of thromboembolic and obstetric pathological phenomena in these patients. We will also describe the intracellular signaling pathways activated by aPL in various cellular subtypes and outline the current evidence linking these pathways to clinical phenotypes. Finally, we will discuss the implications of distinct molecular patterns defining clinical phenotypes of APS patients.

Original languageEnglish (US)
JournalCurrent Rheumatology Reports
Issue number3
StatePublished - Mar 2015


  • Antiphospholipid antibody
  • Antiphospholipid syndrome
  • Cell dysfunction
  • Cellular activation
  • Pregnancy morbidity
  • Signaling pathway
  • Thrombosis

ASJC Scopus subject areas

  • Rheumatology


Dive into the research topics of 'The Journey of Antiphospholipid Antibodies From Cellular Activation to Antiphospholipid Syndrome'. Together they form a unique fingerprint.

Cite this