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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. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic inflammatory disease with high mortality worldwide. The reverse cholesterol transport pathway in macrophage plays an important role in the pathogenesis of coronary artery disease (CAD) and is strongly controlled by regulatory factors. The microRNAs can promote or prevent the formation of atherosclerotic lesions by post‐transcriptional regulation of vital genes in this pathway. Therefore, this study was conducted to investigate the relationship between the expression levels of miR‐27a, miR‐329, ABCA1, and ABCG1 genes and serum levels of hs‐CRP, ox‐LDL, and indices of oxidative stress in the patients with established CAD and controls. A total of 84 subjects (42 patients with CAD and 42 controls) were included in this study. Expression levels of miR‐27a‐3p, miR‐329‐3p, ABCA1, and ABCG1 genes in the peripheral blood mononuclear cells (PBMCs) and serum concentration of hs‐CRP and ox‐LDL were measured by real time‐PCR and ELISA, respectively. Also, oxidative stress parameters in the serum were evaluated by ferric‐reducing antioxidant power (FRAP) and malondialdehyde (MDA) assays. ABCA1 and ABCG1 gene expression in PBMC and serum concentration of FRAP were significantly lower in the CAD group compared to the control group. Expression levels of miR‐27a and miR‐329 and serum levels of hs‐CRP, ox‐LDL, and MDA were significantly higher in the CAD group compared to the control group. Serum levels of hs‐CRP, ox‐LDL, and expression level of miR‐27a have inversely related to ABCA1 and ABCG1 gene expression in all the subjects. An increase in the expression levels of miR‐27a and miR‐329 may lead to the progression of atherosclerosis plaque by downregulating the expression of ABCA1 and ABCG1 genes. [ABSTRACT FROM AUTHOR]