Matsuura Eiji, Kobayashi Kazuko, Lopez Luis R
Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
Autoimmun Rev. 2008 Jan;7(3):214-22. doi: 10.1016/j.autrev.2007.11.008. Epub 2007 Nov 29.
Atherosclerosis is a chronic inflammatory disease of the arteries associated with various risk factors that promote lipid abnormalities (i.e., dyslipidemia), development and progression of atherosclerotic lesions, plaque rupture, and vascular thrombosis. Experimental evidence from biochemical and clinical studies support the idea that arterial thrombosis is an autoimmune process resulting from 'autoantibody'-mediated pro-atherogenic mechanisms now seen in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). In addition, it has been shown that persistent infections of Chlamydia pneumoniae (C. pneumoniae), Porphyromonas gingivalis (P. gingivalis), and Helicobacter pylori (H. pylori) cause immune responses (infectious immunity) in their hosts that promote atherogenesis. In this article, we review recent progress in our understanding of immune- and infection-mediated atherosclerosis.
动脉粥样硬化是一种动脉的慢性炎症性疾病，与多种促进脂质异常（即血脂异常）、动脉粥样硬化病变的发生和发展、斑块破裂及血管血栓形成的危险因素相关。生化和临床研究的实验证据支持这样一种观点，即动脉血栓形成是一种自身免疫过程，由“自身抗体”介导的促动脉粥样硬化机制引起，目前在系统性红斑狼疮（SLE）和抗磷脂综合征（APS）中可见。此外，研究表明，肺炎衣原体（C. pneumoniae）、牙龈卟啉单胞菌（P. gingivalis）和幽门螺杆菌（H. pylori）的持续感染会在其宿主中引发促进动脉粥样硬化的免疫反应（感染免疫）。在本文中，我们综述了在理解免疫和感染介导的动脉粥样硬化方面的最新进展。
