Is atherosclerosis an autoimmune disease?

BMC Medicine

Commentary

Maurizio Turiel¹  Eiji Matsuura²  Luis R Lopez³  Fabiola Atzeni⁴  Piercarlo Sarzi-Puttini⁴  Michael T Nurmohamed⁵ 

[1] Cardiology Unit, Department of Biomedical Sciences for Health, Galeazzi Orthopedic Institute IRCCS, University of Milan, Milan, Italy;Collaborative Research Center (OMIC), Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-cho, 700-8558, Kita-ku, Okayama, Japan;Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan;Medical Department, Corgenix Inc, Broomfield, CO, USA;Rheumatology Unit, L. Sacco University Hospital of Milan, Milan, Italy;VU University Medical Center and Jan van Breemen Research Institute, Amsterdam, The Netherlands;

关键词: Atherosclerosis;    Auto-inflammatory disease;    Autoimmunity;    β2-glycoprotein I;    Innate immunity;    Inflammasome;    Oxidized LDL;   

DOI  :  10.1186/1741-7015-12-47

 received in 2014-02-24, accepted in 2014-02-24,  发布年份 2014

来源: Springer

【 摘 要 】

Immunologic research into pathogenic mechanisms operating in autoimmune-mediated atherosclerosis initially focused on adaptive immunity. Current interest is directed to more basic inflammatory mechanisms. Chronic inflammation (innate immunity-associated) may trigger initial events that can lead to atherosclerotic cardiovascular disease. This chronic inflammation may start early in life and be perpetuated by classic atherosclerosis risk factors. Lipid peroxidation of low-density lipoprotein seems to be a key event in the initiation and progression of atherosclerosis. Oxidized low-density lipoprotein triggers inflammatory and immunogenic events that promote endothelial dysfunction and the synthesis and secretion of pro-inflammatory cytokines, leading to an autoimmune response capable of accelerating the intracellular accumulation of lipids within atherosclerotic plaques. Oxidized low-density lipoprotein binds β2-glycoprotein I to form circulating complexes found in both autoimmune and non-autoimmune atherosclerosis. It is likely that β2-glycoprotein I and/or these complexes contribute to early atherogenesis by stimulating pro-inflammatory innate immunity through endogenous sensors and inflammasome/interleukin-1 pathways. We discuss the chronic inflammatory (innate) and autoimmune (adaptive) responses operating in atherosclerosis to discern the role of autoimmunity in atherosclerotic cardiovascular disease.

【 授权许可】

CC BY   
© Matsuura et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.