Autoantibody-triggered apoptosis of endothelial cells induces antiphospholipid antibody in infectious diseases

Pierre Youinou, Yehuda Shoenfeld

Research output: Contribution to journalReview articlepeer-review


Evidence has long been lacking that antiendothelial cell (EQ antibodies (AECA) are deleterious, but recent studies have kindled a new debate on their pathogenicity, Intriguingly, they may be associated with infectious diseases and/or with antiphospholipid (PL) antibody (aPL). The latter are directed against complexes of anionic PL, such as phosphatidylserine (PS), and PL-binding cationic proteins, most notably P2-glycoprotein I (β2GPI). The mechanism linking the production of pathogenic anti-PL with the presence of AECA is presently unknown. Our hypothesis is that infectious agents generate β 2GPI-independent non-pathogenic anti-PL, and trigger the production of AECA. Some of those encountered in infectious diseases induce EC into apoptosis. They are thus responsible for PS reaching the plasma membrane, a feature for commitment to apoptosis. Defective macrophage clearance of EC undergoing AECA-induced apoptosis prolongs the exposure of PS on their surface, and enables its association with β2GPI. Owing to this boost by AECA, the infection-induced β2GPI-independent and non-pathogenic anti-PL are rendered β2GPI-dependent and pathogenic.

Original languageEnglish
Pages (from-to)11-18
Number of pages8
JournalCurrent Trends in Immunology
StatePublished - 2007


  • Antiendothelial cell antibody
  • Endothelial cell
  • Infectious agent
  • Phopholipid
  • β-glycoprotein I


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