Inflammation and immune system interactions in atherosclerosis
- PDF / 997,725 Bytes
- 23 Pages / 595.276 x 790.866 pts Page_size
- 83 Downloads / 215 Views
Cellular and Molecular Life Sciences
Review
Inflammation and immune system interactions in atherosclerosis Bart Legein · Lieve Temmerman · Erik A. L. Biessen · Esther Lutgens
Received: 24 July 2012 / Revised: 30 January 2013 / Accepted: 4 February 2013 © Springer Basel 2013
Abstract Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.
B. Legein · L. Temmerman · E. A. L. Biessen Experimental Vascular Pathology, Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), University of Maastricht, Universiteitssingel 50, 6229 ER Maastricht, The Netherlands E. Lutgens (*) Experimental Vascular Biology, Department of Medical Biochemistry, Academic Medical Center (AMC), University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands e-mail: [email protected]; [email protected] E. Lutgens Institute for Cardiovascular Prevention (IPEK), Ludwig Maximilian’s University, Pettenkoferstrasse 8a/9, 80336 Munich, Germany
Keywords Atherosclerosis · Innate immune system · Adaptive immune system · Co-stimulation
Introduction The most common underlying cause of cardiovascular diseases, such as myocardial infarction or stroke, is atherosclerosis [1, 2]. Atherosclerosis is a slowly progressing disease in which lesions (plaques) are formed in large and mid-sized arteries. Risk factors are hypertension, diabetes, smoking, and excessive food intake, but also previous infections (influenza, oral pathogens) or underlying (auto) immune diseases like lupus, Wegener’s granulomatosis or rheumatoid arthritis [3–6]. Although plaques can grow to a sufficiently large size to compromise blood flow, most of its clinical complications are attributable to arterial occlusion due to plaque erosion or rupture [7]. Plaques form at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points [7]. In the past two to three decades, experimental and patient studies have fueled the notion that atherosclerosis is a lipid-driven chronic inflammatory disease of the arterial wall in which several components of both
Data Loading...
