IL-18 is involved in the development of atherosclerosis and contributes to plaque instability through an immune response that increases the synthesis of endothelial adhesion molecules by inducing the synthesis of interferon-gamma (IFN-γ) and reduces the size of the fibrous plaque cap by promoting the expression of major histocompatibility complex II (MHC II) on macrophages and vascular cells. Here, IL18 is linked to atherosclerosis.