Abstract
Inflammation plays a key role in the initiation and progression of atherosclerosis and can be caused by multiple agents, including increased concentration of circulating low-density lipoprotein (LDL) cholesterol. Areas of the arterial wall affected by atherosclerosis are enriched with lymphocytes and dendritic cells (DCs). Atherosclerotic plaques contain a variety of proinflammatory immune cells, such as macrophages, DCs, T cells, natural killer cells, neutrophils and others. Intracellular lipid accumulation in atherosclerotic plaque leads to formation of so-called foam cells, the cytoplasm of which is filled with lipid droplets. According to current understanding, these cells can also derive from the immune cells that engulf lipids by means of phagocytosis. Macrophages play a crucial role in the initial stages of atherogenesis by engulfing oxidized LDL (oxLDL) in the intima that leads to their transformation to foam cells. Dying macrophages inside the plaque form a necrotic core that further aggravates the lesion. Proinflammatory DCs prime differentiation of naïve T cells to proinflammatory Th1 and Th17 subsets. In this review, we discuss the roles of cell types of myeloid origin in atherosclerosis-associated inflammation.
Highlights
Atherosclerosis is a common pathology that affects large and medium arteries leading to a variety of cardiovascular events that can be fatal, representing a serious public health problem
Macrophages play a crucial role in the initial stages of atherogenesis by engulfing oxidized low-density lipoprotein (LDL) in the intima that leads to their transformation to foam cells
Ly6high monocytes predominantly move to atherosclerosis-susceptible arteries where they preferentially differentiate to pro-inflammatory macrophages through CX3C chemokine receptor 1 (CX3CR1), chemokine receptor type 2 (CCR2) and CCR5 signaling [20]
Summary
Atherosclerosis is a common pathology that affects large and medium arteries leading to a variety of cardiovascular events that can be fatal, representing a serious public health problem. Atherosclerosis is characterized by progressive lipid deposition in the arterial wall, plaque induction and possible further progression to the state of so-called unstable plaque. Elevated low-density lipoprotein (LDL) is known to be associated with atherosclerosis and is identified as the major source of lipids accumulating in atherosclerotic plaques. Besides elevated LDL, chronic inflammation is considered as another crucial pro-atherogenic mechanism that can even precede lipid entry into the arterial intima [3]. The imbalance of monocyte/macrophage polarization towards the preferential pro-inflammatory phenotype and a lack of normal inflammation resolution are present in atherosclerosis [5]. Failure to resolve the inflammatory response can result in the formation of the most dangerous unstable plaque that can cause thrombosis. We consider main subsets of pro- and anti-inflammatory immune cells of myeloid origin that contribute to atherogenesis
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