Autoantibody-mediated atherosclerosis

Eiji Matsuura, Kazuko Kobayashi, Takao Koike, Yehuda Shoenfeld

Research output: Contribution to journalReview article

49 Citations (Scopus)

Abstract

β2-Glycoprotein I (β2-GPI) is a major antigen for antiphospholipid antibodies (aPL) present in patients with antiphospholipid syndrome (APS). Oxidized low-density lipoprotein (oxLDL) is subsequently targeted by β2-GPI and anti-β2-GPI autoantibodies. Ligands specific for β2-GPI derived from oxLDL have been characterized as oxidized forms of cholesteryl linoleate, such as 7-ketocholesterol-9-carboxynonanoate, i.e. 9-oxo-9-(7-ketocholest-5-en-3β- yloxy) nonanoic acid, (namely oxLig-1). The in vitro phenomenon that it is significantly increased in binding of oxLig-1 containing liposomes to macrophages via an interaction with β2-GPI and an anti-β2-GPI autoantibody (via the Fcγ receptor) may propose a novel mechanism on 'autoantibody-mediated athrosclerosis'. Furthermore, autoantibodies against a complex of β2-GPI and oxLig-1 are detected in sera of APS patients and appearance of the antibodies is associated with episodes of thrombosis, especially, arterial thrombosis. Thus, autoimmune atherogenesis linked to β2-GPI interaction with oxLDL and autoantibodies may be present in APS.

Original languageEnglish
Pages (from-to)348-353
Number of pages6
JournalAutoimmunity Reviews
Volume1
Issue number6
DOIs
Publication statusPublished - Dec 1 2002

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Keywords

  • Anti-β-glycoprotein I antibody
  • Antiphospholipid syndrome
  • Autoantibody
  • Macrophage
  • Oxidized LDL
  • β-Glycoprotein

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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