Mechanisms of atherosclerosis--a review

The response-to-injury hypothesis of atherosclerosis takes into account interactions among all of the cells found in the lesions of human atherosclerosis, the cytokines and growth factors that can be formed by each of these cells (which are in fact formed in vitro and which have been demonstrated in vivo). It should therefore be possible to develop new diagnostic tools that will help us to make early diagnoses for patients who are at risk and determine the state of lesion formation in these patients. An intriguing question that remains is the role of the T lymphocytes in these lesions. The presence of these cells, and some early preliminary data, indicating that antigens unique to the lesions of atherosclerosis are present in the lesions, suggest that many of the lesions of atherosclerosis represent immune or autoimmune responses. The nature of the antigens, the response to these antigens, and the role of antigen-antibody complexes in the process of atherogenesis are important questions to be answered before we reach an understanding of this complex disease process that causes 50% of all deaths in the United States and Western Europe.