Arterial inflammation is a significant component of atherosclerotic disease and it has been suggested that specific immune responses directed against autoantigens or pathogen-derived antigens presented in the vascular wall could initiate and/or maintain atherosclerotic processes. Atherogenic cofactors such as altered cholesterol metabolism may not only impact locally on inflammatory responses in atherosclerotic lesions, but may also alter general immune-responsiveness. The evidence to date suggests that the mutual chronic perpetuation of immune mediated vascular inflammation and cholesterol-induced atherosclerosis is a key step in atherogenesis.