Anti-β2 glycoprotein I antibodies prevent the de-activation of platelets and sustain their phagocytic clearance

Attilio Bondanza, Maria Grazia Sabbadini, Fabio Pellegatta, Valérie S. Zimmermann, Angela Tincani, Genesio Balestrieri, Angelo A. Manfredi, Patrizia Rovere

Research output: Contribution to journalArticle


Exposure to phosphatidylserine (PS) tags dying and senescent cells for removal and identifies activated platelets. In this study we followed the fate of PS-exposing platelets in the presence of antibodies purified from Systemic Lupus Erythematosus (SLE) and primary Anti-phospholipid Syndrome (APS) patients' sera by β2GPI affinity chromatography. Thrombin-activated platelets exposed PS and associated to β2GPI. Both events were required for recognition by antibodies. Human monocyte-derived macrophages phagocytosed activated platelets only. Each macrophage internalized an average of 3.16±0.2 platelets after 60 min at 37°C. Phagocytosis did not increase after longer incubations (4.65±0.26 platelets internalized by each macrophage after 300 min). Recognition of platelets by anti-β2GPI antibodies significantly increased phagocytosis (P1200 min). The ability to phagocytose opsonized platelets was accordingly sustained (5.3±0.2 opsonized platelets were internalized by each macrophage after 60 min and 9.4±.0.3 after 300 min). Anti-β2GPI antibodies therefore poise activated platelets in a PS-exposing status, preventing the recycling of their function and favoring their phagocytic clearance. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)469-477
Number of pages9
JournalJournal of Autoimmunity
Issue number4
Publication statusPublished - 2000



  • Anti-β2 glycoprotein I antibodies
  • Phagocytosis
  • Phosphatidylserine
  • Platelets

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this