Immunogenic oxidized low-density lipoprotein/β2-glycoprotein I complexes in the diagnostic management of atherosclerosis

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

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Oxidized low-density lipoprotein (oxLDL) promotes atherosclerosis through a complex interaction of inflammatory and immunologic factors that lead to macrophage lipid uptake and foam cell formation. OxLDL interacts with β2-glycoprotein I (β2GPI) forming oxLDL/β2GPI complexes. These complexes may be formed in the arterial intima during atherogenesis and released into the circulation. Autoantibodies against oxLDL/β2GPI complexes have been demonstrated in patients with systemic lupus erythematosus and/or antiphospholipid syndrome, and shown to be significantly associated with arterial thrombosis. The observation that monoclonal autoantibodies against oxLDL/β2GPI complexes significantly increased the oxLDL uptake by macrophages strongly suggests that such IgG autoantibodies are pro-atherogenic. In this article, we review the recent progress in our understanding of LDL oxidation, oxLDL/β2GPI complex formation, and immune regulation of atherogenesis.

Original languageEnglish
Pages (from-to)12-19
Number of pages8
JournalClinical Reviews in Allergy and Immunology
Volume37
Issue number1
DOIs
Publication statusPublished - 2009

Fingerprint

LDL Lipoproteins
Atherosclerosis
Glycoproteins
Autoantibodies
Macrophages
Tunica Intima
Foam Cells
Antiphospholipid Syndrome
oxidized low density lipoprotein
Immunologic Factors
Antigen-Antibody Complex
Systemic Lupus Erythematosus
Thrombosis
Immunoglobulin G
Lipids

Keywords

  • Antiphospholipid antibodies
  • Atherosclerosis
  • Autoimmunity
  • Oxidized LDL
  • β2GPI

ASJC Scopus subject areas

  • Immunology and Allergy
  • Medicine(all)

Cite this

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abstract = "Oxidized low-density lipoprotein (oxLDL) promotes atherosclerosis through a complex interaction of inflammatory and immunologic factors that lead to macrophage lipid uptake and foam cell formation. OxLDL interacts with β2-glycoprotein I (β2GPI) forming oxLDL/β2GPI complexes. These complexes may be formed in the arterial intima during atherogenesis and released into the circulation. Autoantibodies against oxLDL/β2GPI complexes have been demonstrated in patients with systemic lupus erythematosus and/or antiphospholipid syndrome, and shown to be significantly associated with arterial thrombosis. The observation that monoclonal autoantibodies against oxLDL/β2GPI complexes significantly increased the oxLDL uptake by macrophages strongly suggests that such IgG autoantibodies are pro-atherogenic. In this article, we review the recent progress in our understanding of LDL oxidation, oxLDL/β2GPI complex formation, and immune regulation of atherogenesis.",
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AB - Oxidized low-density lipoprotein (oxLDL) promotes atherosclerosis through a complex interaction of inflammatory and immunologic factors that lead to macrophage lipid uptake and foam cell formation. OxLDL interacts with β2-glycoprotein I (β2GPI) forming oxLDL/β2GPI complexes. These complexes may be formed in the arterial intima during atherogenesis and released into the circulation. Autoantibodies against oxLDL/β2GPI complexes have been demonstrated in patients with systemic lupus erythematosus and/or antiphospholipid syndrome, and shown to be significantly associated with arterial thrombosis. The observation that monoclonal autoantibodies against oxLDL/β2GPI complexes significantly increased the oxLDL uptake by macrophages strongly suggests that such IgG autoantibodies are pro-atherogenic. In this article, we review the recent progress in our understanding of LDL oxidation, oxLDL/β2GPI complex formation, and immune regulation of atherogenesis.

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