In recent years, it has been shown that in¯ammation plays an important role in the pathogenesis of atherosclerosis. Activated macrophages, T lymphocytes, and mast cells are present in atherosclerotic plaques, which has led to the notion that the in¯ammatory response is an immunemediated process. Complicated lesions, moreover, appear to be associated with an increase in the amount of the in¯ammatory response and in these patients, increased levels of acute phase proteins are present. The appreciation that atherosclerosis is an immune-mediated in¯ammatory disease has also led to renewed interest in the potential role of infectious agents in initiating or modulating atherosclerosis. Seroepidemiological studies have shown raised antibody titres against several micro-organisms. However, as yet, there are hardly any data available that provide a sound scienti®c basis for an infectious origin. Of all potential candidate organisms, Chlamydia pneumoniae appears as the one most likely involved in atherogenesis. C. pneumoniae has been retrieved from atherosclerotic tissues; the level of raised plasma titres correlates with the severity of symptomatic atherosclerotic disease; and the incidence of C. pneumoniae-responsive T cells in peripheral blood is increased in patients with coronary heart disease. It also appears that in some patients T cells generated from atherosclerotic plaques respond to C. pneumoniae. At the present state of knowledge, however, it is fair to state that the relationship between infection, intraplaque in¯ammation, and atherosclerosis still remains hypothetical, despite the increasing evidence that such a relationship could exist.