An overview of the innate and adaptive immune system in atherosclerosis. Issue 1 (7th December 2020)

• Record Type: Journal Article
• Authors: Mohmmad‐Rezaei, Mina; Arefnezhad, Reza; Ahmadi, Reza; Abdollahpour‐Alitappeh, Meghdad; Mirzaei, Yousef; Arjmand, Mohammad‐Hassan; Ferns, Gordon A.; Bashash, Davood; Bagheri, Nader
• Is Part Of: IUBMB life. Volume 73:Issue 1(2021)
• Page Start: 64
• Page End: 91
• Publication Date: 2020-12-07
• Subjects: adaptive immune systems -- atherosclerosis -- innate immune system; Biochemistry -- Periodicals; Molecular biology -- Periodicals; 572.8
• DOI: 10.1002/iub.2425
• Languages: English
• ISSNs: 1521-6543

Abstract

Abstract: Cardiovascular disease is the leading cause of death globally. Coronary artery disease (CAD) is a chronic inflammatory disease usually caused by atherosclerosis, in which the coronary arteries become narrowed by atheromatous plaque. Plaques in atherosclerosis are formed through the accumulation of lipids and various immune cells. Both adaptive and innate immune systems are involved in the pathogenesis of atherosclerosis and facilitate plaque formation and disease progression. Almost all immune system cells, including neutrophils, B cells, T cells monocytes, macrophages, foam cells, and dendritic cells (DCs), play a vital role in atherosclerotic plaque. Atherogenesis, the normal function of the endothelium, is initially disrupted and, then, cells of the immune system are recruited to the endothelium following increased expression of cell adhesion molecules. Accumulation of immune cells and lipids leads to the formation of a necrotic nucleus. As the disease progresses, smooth muscle cells form fibrous layers, whose rupture results in exposing the necrotic nucleus and thrombosis. Accordingly, the present review was conducted to determine the role of different cells in innate and adaptive immune systems in inhibition and progression of atherosclerosis.