Atherosclerosis is an inflammatory disease of large and medium-sized arteries, primarily driven by elevated levels of low-density lipoprotein (LDL) cholesterol. In atherosclerotic arteries, immune cells such as dendritic cells (DCs), macrophages, and lymphocytes are present in higher numbers and different distributions compared to normal arteries. These cells contribute to the formation of atherosclerotic plaques, which consist of necrotic cores, calcified regions, modified lipids, and inflammatory cells. The progression of atherosclerosis involves the recruitment and retention of immune cells, their activation, and the production of pro- and anti-inflammatory mediators. Experimental interventions that reduce the number of blood monocytes can decrease atherosclerotic lesion burden without affecting blood lipids. Proatherogenic conditions reduce nitric oxide production and increase reactive oxygen species (ROS) and advanced glycation end products (AGE). Inhibiting ROS-generating NADPH oxidase or the AGE receptor (RAGE) has beneficial effects. Targeting inflammatory adhesion molecules also reduces atherosclerosis. Conversely, removing or blocking IL-10 or TGF-β accelerates atherosclerosis. Regulatory T cells and B1 cells secreting natural antibodies are atheroprotective. This review summarizes the current understanding of inflammatory and immune mechanisms in atherosclerosis, including the roles of inflammatory cells, their recruitment and retention in atherosclerotic plaques, and the regulation of atherosclerosis by pro- and anti-inflammatory mediators. The review also discusses the association of atherosclerosis with other inflammatory diseases and potential anti-inflammatory treatments. Key immune cells involved in atherosclerosis include macrophages, DCs, T lymphocytes, B cells, and natural killer (NK) cells. Macrophages can be polarized into M1 (pro-inflammatory) or M2 (anti-inflammatory) subtypes. Monocyte subsets, such as Ly6C high and Ly6C low, have distinct roles in atherosclerosis. Vascular DCs are found in atherosclerotic lesions and may present antigens to T cells. T lymphocytes, including CD4+ and CD8+ T cells, play a role in atherosclerosis, with Th1 and Th2 responses contributing to disease progression. Regulatory T cells (Tregs) help maintain immunological tolerance and reduce atherosclerosis. γδ T cells, natural killer T cells, and mast cells also contribute to atherosclerosis. Cytokines such as TNF-α, IL-1, IL-6, IL-12, IL-18, and IFN-γ are involved in the inflammatory processes of atherosclerosis. The balance between Th1 and Th2 responses is regulated by Tregs. Obesity and diabetes are associated with atherosclerosis, with adipokines such as adiponectin and leptin playing roles in inflammation and lipid metabolism.Atherosclerosis is an inflammatory disease of large and medium-sized arteries, primarily driven by elevated levels of low-density lipoprotein (LDL) cholesterol. In atherosclerotic arteries, immune cells such as dendritic cells (DCs), macrophages, and lymphocytes are present in higher numbers and different distributions compared to normal arteries. These cells contribute to the formation of atherosclerotic plaques, which consist of necrotic cores, calcified regions, modified lipids, and inflammatory cells. The progression of atherosclerosis involves the recruitment and retention of immune cells, their activation, and the production of pro- and anti-inflammatory mediators. Experimental interventions that reduce the number of blood monocytes can decrease atherosclerotic lesion burden without affecting blood lipids. Proatherogenic conditions reduce nitric oxide production and increase reactive oxygen species (ROS) and advanced glycation end products (AGE). Inhibiting ROS-generating NADPH oxidase or the AGE receptor (RAGE) has beneficial effects. Targeting inflammatory adhesion molecules also reduces atherosclerosis. Conversely, removing or blocking IL-10 or TGF-β accelerates atherosclerosis. Regulatory T cells and B1 cells secreting natural antibodies are atheroprotective. This review summarizes the current understanding of inflammatory and immune mechanisms in atherosclerosis, including the roles of inflammatory cells, their recruitment and retention in atherosclerotic plaques, and the regulation of atherosclerosis by pro- and anti-inflammatory mediators. The review also discusses the association of atherosclerosis with other inflammatory diseases and potential anti-inflammatory treatments. Key immune cells involved in atherosclerosis include macrophages, DCs, T lymphocytes, B cells, and natural killer (NK) cells. Macrophages can be polarized into M1 (pro-inflammatory) or M2 (anti-inflammatory) subtypes. Monocyte subsets, such as Ly6C high and Ly6C low, have distinct roles in atherosclerosis. Vascular DCs are found in atherosclerotic lesions and may present antigens to T cells. T lymphocytes, including CD4+ and CD8+ T cells, play a role in atherosclerosis, with Th1 and Th2 responses contributing to disease progression. Regulatory T cells (Tregs) help maintain immunological tolerance and reduce atherosclerosis. γδ T cells, natural killer T cells, and mast cells also contribute to atherosclerosis. Cytokines such as TNF-α, IL-1, IL-6, IL-12, IL-18, and IFN-γ are involved in the inflammatory processes of atherosclerosis. The balance between Th1 and Th2 responses is regulated by Tregs. Obesity and diabetes are associated with atherosclerosis, with adipokines such as adiponectin and leptin playing roles in inflammation and lipid metabolism.