Atherosclerosis is an inflammatory disease of large- and medium-sized arteries, characterized by the accumulation of lipids, immune cells, and fibrous tissue. The disease is initiated by elevated levels of low-density lipoprotein (LDL) cholesterol in the blood and is characterized by the recruitment and activation of immune cells, including dendritic cells (DCs), lymphocytes, macrophages, and foam cells. Experimental interventions that reduce the number of blood monocytes, which are the source of macrophages and DCs, can decrease atherosclerotic lesion burden without altering blood lipids. Under proatherogenic conditions, nitric oxide production from endothelial cells is reduced, and reactive oxygen species (ROS) and advanced glycation end products (AGEs) are increased. Targeting inflammatory adhesion molecules and regulatory T cells, as well as B1 cells secreting natural antibodies, can reduce atherosclerosis. This review summarizes the current understanding of inflammatory and immune mechanisms in atherosclerosis, including the role of various immune cells, cytokines, chemokines, and other mediators.Atherosclerosis is an inflammatory disease of large- and medium-sized arteries, characterized by the accumulation of lipids, immune cells, and fibrous tissue. The disease is initiated by elevated levels of low-density lipoprotein (LDL) cholesterol in the blood and is characterized by the recruitment and activation of immune cells, including dendritic cells (DCs), lymphocytes, macrophages, and foam cells. Experimental interventions that reduce the number of blood monocytes, which are the source of macrophages and DCs, can decrease atherosclerotic lesion burden without altering blood lipids. Under proatherogenic conditions, nitric oxide production from endothelial cells is reduced, and reactive oxygen species (ROS) and advanced glycation end products (AGEs) are increased. Targeting inflammatory adhesion molecules and regulatory T cells, as well as B1 cells secreting natural antibodies, can reduce atherosclerosis. This review summarizes the current understanding of inflammatory and immune mechanisms in atherosclerosis, including the role of various immune cells, cytokines, chemokines, and other mediators.