Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity
Identifieur interne : 000798 ( Pmc/Corpus ); précédent : 000797; suivant : 000799Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity
Auteurs : Nicolas Vuilleumier ; Fabrizio Montecucco ; Oliver HartleySource :
- World Journal of Cardiology [ 1949-8462 ] ; 2014.
Abstract
Immune-driven inflammation plays an important part in atherogenesis and is therefore believed to be key to the development of cardiovascular disease (CVD), which is currently the leading cause of death in the Western world. By fulfilling some of the Koch postulates, atherogenesis has even been proposed to be considered as an autoimmune disease, raising the hope that CVD could be prevented by immunomodulation. Nevertheless, the role of the immune system and autoimmune reactions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenic attributes. Hence, if immunomodulation is to become a therapeutic option for atherosclerosis and CVD, it will be crucial to correctly identify patients who might benefit from targeted suppression of deleterious autoimmune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clinical, in vitro, and animal studies dedicated to autoantibodies 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,
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DOI: 10.4330/wjc.v6.i5.314
PubMed: 24944761
PubMed Central: 4062126
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PMC:4062126Le document en format XML
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<author><name sortKey="Vuilleumier, Nicolas" sort="Vuilleumier, Nicolas" uniqKey="Vuilleumier N" first="Nicolas" last="Vuilleumier">Nicolas Vuilleumier</name>
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<author><name sortKey="Montecucco, Fabrizio" sort="Montecucco, Fabrizio" uniqKey="Montecucco F" first="Fabrizio" last="Montecucco">Fabrizio Montecucco</name>
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<series><title level="j">World Journal of Cardiology</title>
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<front><div type="abstract" xml:lang="en"><p>Immune-driven inflammation plays an important part in atherogenesis and is therefore believed to be key to the development of cardiovascular disease (CVD), which is currently the leading cause of death in the Western world. By fulfilling some of the Koch postulates, atherogenesis has even been proposed to be considered as an autoimmune disease, raising the hope that CVD could be prevented by immunomodulation. Nevertheless, the role of the immune system and autoimmune reactions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenic attributes. Hence, if immunomodulation is to become a therapeutic option for atherosclerosis and CVD, it will be crucial to correctly identify patients who might benefit from targeted suppression of deleterious autoimmune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clinical, in vitro, and animal studies dedicated to autoantibodies 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, <italic>in vitro</italic>
and animal studies indicate a pro-inflammatory and pro-atherogenic role, supporting 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.</p>
</div>
</front>
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<pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">World J Cardiol</journal-id>
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<journal-title-group><journal-title>World Journal of Cardiology</journal-title>
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<issn pub-type="ppub">1949-8462</issn>
<issn pub-type="epub">1949-8462</issn>
<publisher><publisher-name>Baishideng Publishing Group Inc</publisher-name>
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<article-id pub-id-type="doi">10.4330/wjc.v6.i5.314</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
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<title-group><article-title>Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Vuilleumier</surname>
<given-names>Nicolas</given-names>
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<contrib contrib-type="author"><name><surname>Montecucco</surname>
<given-names>Fabrizio</given-names>
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<contrib contrib-type="author"><name><surname>Hartley</surname>
<given-names>Oliver</given-names>
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<aff>Nicolas Vuilleumier, Fabrizio Montecucco, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 1211 Geneva, Switzerland</aff>
<aff>Nicolas Vuilleumier, Fabrizio Montecucco, Department of Human Protein Sciences, Faculty of Medicine, 1211 Geneva, Switzerland</aff>
<aff>Fabrizio Montecucco, Department of Internal Medicine, Foundation for Medical Researches, Faculty of Medicine, Geneva 1211, Switzerland</aff>
<aff>Oliver Hartley, Department of Immunology and Pathology, Faculty of Medicine, 1211 Geneva, Switzerland</aff>
</contrib-group>
<author-notes><fn><p>Author contributions: All the authors contributed to this manuscript.</p>
<p>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. <email>nicolas.vuilleumier@hcuge.ch</email>
</p>
<p>Telephone: +41-22-3729150 Fax: +41-22-3827245</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><day>26</day>
<month>5</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>26</day>
<month>5</month>
<year>2014</year>
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<volume>6</volume>
<issue>5</issue>
<fpage>314</fpage>
<lpage>326</lpage>
<history><date date-type="received"><day>23</day>
<month>12</month>
<year>2013</year>
</date>
<date date-type="rev-recd"><day>5</day>
<month>2</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>17</day>
<month>3</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>©2014 Baishideng Publishing Group Inc. All rights reserved.</copyright-statement>
<copyright-year>2014</copyright-year>
</permissions>
<abstract><p>Immune-driven inflammation plays an important part in atherogenesis and is therefore believed to be key to the development of cardiovascular disease (CVD), which is currently the leading cause of death in the Western world. By fulfilling some of the Koch postulates, atherogenesis has even been proposed to be considered as an autoimmune disease, raising the hope that CVD could be prevented by immunomodulation. Nevertheless, the role of the immune system and autoimmune reactions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenic attributes. Hence, if immunomodulation is to become a therapeutic option for atherosclerosis and CVD, it will be crucial to correctly identify patients who might benefit from targeted suppression of deleterious autoimmune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clinical, in vitro, and animal studies dedicated to autoantibodies 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, <italic>in vitro</italic>
and animal studies indicate a pro-inflammatory and pro-atherogenic role, supporting 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.</p>
</abstract>
<kwd-group><kwd>Autoantibodies</kwd>
<kwd>Cardiovascular disease</kwd>
<kwd>Atherosclerosis</kwd>
<kwd>Apolipoprotein A-1</kwd>
<kwd>Autoimmunity</kwd>
<kwd>Biomarkers</kwd>
</kwd-group>
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