Although inflammation has been known to play a role in cardiovascular disease (CVD) for decades, increasing evidence suggests that certain factors leading to atherosclerosis could be partly due to autoimmunity. Nilsson and Hansson reviewed the literature on this topic in the latest issue of the Journal of Internal Medicine. One possible mechanism linking autoantigens and atherosclerosis is the production of specific antigens for modified lipoproteins. Although modified LDL initiates the pathology of atherosclerosis, the inflammatory response that it generates could be as harmful to the vascular endothelium as the lipoproteins themselves. Indeed, when they reach the intima of the arterial wall, these lipoproteins become oxidized (oxLDL) and can be taken by dendritic cells, which migrate to lymph nodes and present oxLDL-derived antigens to naive T cells. As a result, about 10% of all T cells in human atherosclerotic plaques are specific to oxLDL particles. As with other autoimmune or chronic diseases such as type 1 diabetes, rheumatoid arthritis, multiple sclerosis, and many others, therapeutic approaches that target the immune system to potentially “cure” CVD remain to be tested in humans. Promising results, which are mentioned in the review, have been obtained in mice. The authors carefully conclude that although many difficulties can be expected in transferring knowledge obtained with experimental animals to humans, it is reasonable to anticipate that a number of vaccines and other immunomodulatory treatments for atherosclerosis will be available within the next few years. Seven other reviews on the topic of atherosclerosis and inflammation were also published in the same issue of the Journal of Internal Medicine.
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