Figure 1: Immune response in atherosclerosis. Macrophages and dendritic cells are the important components of innate immune response in atherosclerosis. Uptake of modified LDL particles such as oxLDL through scavenger receptors leads to the intracellular accumulation of cholesterol leading to activation and expression of a series of genes encoding proinflammatory molecules, including cytokines, chemokines, eicosanoids, proteases, oxidases, and costimulatory molecules. Adaptive immune response is activated when self-antigens, oxidized LDL, and other disease-related antigens are presented to T cells by the macrophages/dendritic cells. The concomitant release of cytokines determines the maturation of the T cell recognizing the antigen. Differentiation into Th1 cells results in inflammatory response, while Th2 leads to activation of antigen-specific B cells. These B cells produce antibodies to the disease-specific antigens. Regulatory T cells induce a tolerogenic response mediated by Tr1 cells and Th3 cells which secrete IL10 and TGF-β respectively, which inhibit the progression of the disease. Th, T helper cells; Treg, regulatory T cell; IL, interleukin; VEGF, vascular endothelial growth factor; TNF, tumor necrosis factor; MIF, migration inhibition factor; Ox-LDL, oxidized low-density lipoprotein; HSP, heat shock protein, CETP, cholesteryl ester transfer protein.