Model of the Development of Arteriosclerosis. (1) Low-density lipoprotein (LDL) moves into the subendothelial space and becomes oxidized. (2) Inflammatory cells are recruited into the vessel wall via induced endothelial adhesion molecules (VCAM, ICAM) and (3) take up oxidized LDL and become foam cells. (4) Activation of macrophages leads to the release of inflammatory cytokines, chemokines, inflammatory molecules and reactive oxygen species leading to (5) the perpetuation of inflammation and tissue damage. (6) Antigens presented by macrophages and dendritic cells trigger the activation of cytotoxic T-cells, which produce Th-1 cytokines and heat-shock proteins as well as TGF-β, which activates smooth-muscle cells (7).