I t is now widely accepted that inflammation and immunity play important roles in the pathogenesis of atherosclerosis and diabetes mellitus. Over the past 3 decades, it has been demonstrated that cells of both the innate and adaptive immune systems contribute to the progression of atherosclerosis and modulation of plaque stability. Similarly, recent studies in experimental models of obesity and type II diabetes mellitus have shown that not only macrophages, but also T cells and B cells are involved in the modulation of adipose depots and the development of insulin resistance. 2-5 However, even with all that is known about the important cellular players in atherogenesis, a clear understanding of the mechanisms by which immune cells influence arterial plaque formation is lacking.
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Major et al. (2011) studied this question.
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