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Lupus
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Reviews

Autoimmunity in atherosclerosis: lessons from experimental models

J George

Department of Medicine ‘B’ and the Research Unit of Autoimmune Diseases, Tel-Aviv University, Tel-Aviv, Israel

A Afek

Institute of Pathology Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

B Gilburd

Department of Medicine ‘B’ and the Research Unit of Autoimmune Diseases, Tel-Aviv University, Tel-Aviv, Israel

D Harats

Lipid and Atherosclerosis Research, Sheba Medical Center, Tel-Hashomer, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

Y Shoenfeld

Department of Medicine ‘B’ and the Research Unit of Autoimmune Diseases, Tel-Aviv University, Tel-Aviv, Israel; Department of Medicine ‘B’, Sheba Medical Center, Tel-Hashomer 52621, Israel. Tel: (+972) 3 5302652; Fax: (+972) 3 535 2855; shoenfel{at}post,tau,ac.il

The modern view of atherosclerosis is of a chronic inflammatory disorder. In accord with this paradigm, the process of uninhibited influx of fat to the vessel wall results from an ‘adequate’ response to various forms of injury (i.e. turbulence, infections, modified lipoproteins). This idea has been further extended by several groups, to assume that the atherosclerotic lesion can be the target of an autoimmune mediated attack. According to this hypothesis, the site of initiation of the plaque should bear/express the target autoantigen, whereas concomitantly a respective immune response is generated in the periphery. The examples illuminating this notion are ß2GPI as a target autoantigen, HSP60/65 an oxidized-LDL.

Herein we present evidence to support the involvement of autoimmune mechanisms in atherogenesis based on the experience from experimental models and human studies.

Key Words: atherosclerosis • antiphospholipid antibodies • autoimmunity • ß2-glycoprotein I • HSP 60/65 • oxLDL

Lupus, Vol. 9, No. 3, 223-227 (2000)
DOI: 10.1191/096120300678828190


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