Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity

Immune-driven inflammation plays an important part inatherogenesis and is therefore believed to be key to thedevelopment of cardiovascular disease(CVD), whichis currently the leading cause of death in the Westernworld. By fulfilling some of the Koch postulates, athero-genesis has even been proposed...

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Published inWorld journal of cardiology Vol. 6; no. 5; pp. 314 - 326
Main Authors Vuilleumier, Nicolas, Montecucco, Fabrizio, Hartley, Oliver
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Inc 26.05.2014
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Summary:Immune-driven inflammation plays an important part inatherogenesis and is therefore believed to be key to thedevelopment of cardiovascular disease(CVD), whichis currently the leading cause of death in the Westernworld. By fulfilling some of the Koch postulates, athero-genesis has even been proposed to be considered as anautoimmune disease, raising the hope that CVD couldbe prevented by immunomodulation. Nevertheless,the role of the immune system and autoimmune reac-tions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenicattributes. Hence, if immunomodulation is to becomea therapeutic option for atherosclerosis and CVD, it willbe crucial to correctly identify patients who might ben-efit from targeted suppression of deleterious autoim-mune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clini-cal, in vitro, and animal studies dedicated to autoan-tibodies against apolipoprotein A-1(anti-apoA-1 IgG), the major proteic fraction of high density lipoprotein. Current clinical studies indicate that high levels of anti-apoA-1 IgG are associated with a worse cardiovascular prognosis. In addition, in vitro and animal studies indi-cate a pro-inflammatory and pro-atherogenic role, sup-porting the hypothesis that these autoantibodies may play a direct causal role in CVD, and furthermore that they could potentially represent a therapeutic target for CVD in the future.
Bibliography:Nicolas Vuilleumier;Fabrizio Montecucco;Oliver Hartley;Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 1211 Geneva, Switzerland;Department of Human Protein Sciences, Faculty of Medicine, 1211 Geneva, Switzerland;Department of Internal Medicine, Foundation for Medical Researches, Faculty of Medicine, Geneva 1211, Switzerland;Department of Immunology and Pathology, Faculty of Medicine, 1211 Geneva, Switzerland
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Author contributions: All the authors contributed to this manuscript.
Telephone: +41-22-3729150   Fax: +41-22-3827245
Correspondence to: Dr. Nicolas Vuilleumier, MD, PD, Head of Laboratory Medicine Division, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 4 rue Gabrielle-Perret-Gentil, 1211 Geneva, Switzerland. nicolas.vuilleumier@hcuge.ch
ISSN:1949-8462
1949-8462
DOI:10.4330/wjc.v6.i5.314