Figure 2: Immune response to LDL in atherosclerosis. The low-density lipoprotein (LDL) in the blood diffuses into the intima of the-vessel wall, where it gets oxidized by enzymes or reactive oxygen to form OxLDL. Modified LDL particles are taken up by macrophages that accumulate cholesterol and become foam cells. Ox-LDL causes overexpression of VCAM-1 and ICAM-1 by the endothelial cells, which attracts the monocytes, and T cells move into the vessel wall. Activated macrophages secrete proinflammatory mediators, such as TNFα, IL-1, MCP-1, and proteolytic enzymes (MMPs). Foam cells can process and present ApoB100 peptides to CD4+ T helper cells via MHC class II molecules. Antigen presentation to CD4+ TH1 cells triggers their activation, with ensuing release of IFN- and TNF known to have proatherogenic properties. VCAM, vascular cell adhesion molecule; ICAM, intercellular cell adhesion molecule; TNF, tumour necrosis factor; IL, interleukin; MCP, macrophage chemoattractant protein; MMP, matrix metalloproteinase, Th, T helper cells; ApoB, apolipoprotein B.