Modulation of endothelial cell function by antiphospholipid antibodies

Lupus. 1996 Oct;5(5):448-50. doi: 10.1177/096120339600500523.

Abstract

beta 2-glycoprotein I (beta 2-GP-I) the plasma cofactor for anti-phospholipid antibodies adheres on the endothelial surfaces and can be recognized by anti-beta 2-GP-I antibodies naturally occurring in patients with the anti-phospholipid syndrome. As for the cofactor binding to cardiolipin- or gamma irradiated-plates, the endothelial binding is mediated by the so-called phospholipid binding site, a cationic structure able to react with anionic molecules. Endothelial monolayers appear to represent a substrate able to bind beta 2-GP-I and to present it in a suitable manner in order to allow the binding of anti-beta 2-GP-I beta 2 antibodies. The complex between beta 2-GP-I and the respective antibodies induce an endothelial cell activation as demonstrated by the up-regulation of adhesion molecule expression, the secretion of proinflammatory cytokines and the modulation of arachidonic acid metabolism. Taken together these findings strongly sustain a pivotal role for beta 2-GP-I in allowing antibody deposition on the endothelium and in affecting endothelial cell functions potentially responsible for a procoagulant state.

MeSH terms

  • Antibodies, Antiphospholipid / physiology*
  • Endothelium, Vascular / physiology*
  • Glycoproteins / immunology
  • Humans
  • Thrombosis / etiology
  • beta 2-Glycoprotein I

Substances

  • Antibodies, Antiphospholipid
  • Glycoproteins
  • beta 2-Glycoprotein I