The immunology of atherothrombosis in the antiphospholipid syndrome: Antigen presentation and lipid intracellular accumulation

Eiji Matsuura, Kazuko Kobayashi, Yukana Matsunami, Luis R. Lopez

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

The antiphospholipid syndrome (APS), characterized by elevated serum levels of antiphospholipid antibodies (aPL) and thromboembolic complications, is a common cause of acquired hypercoagulability. The plasma protein β2-glycoprotein I (β2GPI) is the most clinically relevant antigenic target for aPL. Recent experimental evidence from our laboratory substantiated the concept that IgG anti-β2GPI immune complexes containing oxidized LDL (oxLDL) not only facilitated the intracellular accumulation of oxLDL in macrophages but also allowed the presentation of β2GPI epitopes to pathogenic autoreactive T cells. Both mechanisms required FcγRI-mediated uptake by macrophages/monocytes. Furthermore, several clinical studies demonstrated that the presence of circulating oxLDL/β2GPI complexes and IgG autoantibodies to these complexes was significantly associated with vascular inflammation (i.e. autoimmune-mediated atherothrombosis) in autoimmune patients. In this article, we review recent findings concerning the biochemical and immunologic mechanisms involved in autoimmune-mediated atherothrombosis in patients with APS.

Original languageEnglish
Pages (from-to)500-505
Number of pages6
JournalAutoimmunity Reviews
Volume8
Issue number6
DOIs
Publication statusPublished - May 2009

Keywords

  • Antigen presentation
  • Antiphospholipid syndrome (APS)
  • Atherothrombosis
  • Oxidized LDL (oxLDL)
  • β2-glycoprotein I (β2GPI)

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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