Key Points Atherosclerosis is an inflammatory disease of blood vessels. By causing myocardial infarction and stroke, it is a major cause of death globally. Accumulation of cholesterol-containing plasma lipoproteins triggers inflammation in the artery wall, which can lead to atherosclerosis. Monocyte-derived macrophages accumulate in the early atherosclerotic plaques. Pattern-recognition receptors mediate cholesterol accumulation and inflammatory activation in plaque macrophages. T cells enter plaques at an early stage and, importantly, contribute to plaque progression. T-helper-1 cytokines (such as interferon-γ) and CD40 ligand are strongly pro-atherogenic, as they promote macrophage and endothelial-cell activation, platelet aggregation and thrombosis Regulatory T cells producing immunomodulatory cytokines (such as transforming growth factor-β and interleukin-10) reduce the progression of atherosclerosis. Systemic humoral immunity to oxidized lipoproteins also inhibits disease progression. The long silent phase of atherosclerosis is characterized by smouldering inflammation in plaques. Activation of this pro-inflammatory process can cause plaque activation, rupture and thrombosis. This leads to clinical syndromes such as myocardial infarction and stroke.
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