Immune-Inflammatory Responses in Atherosclerosis: The Role of Myeloid Cells

Journal of Clinical Medicine - Tập 8 Số 11 - Trang 1798
Dimitry A. Chistiakov1, Dmitry Kashirskikh1, Victoria A. Khotina1, Andrey V. Grechko2, Alexander N. Orekhov3,1
1Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315, Moscow, Russia
2Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 109240 Moscow, Russia
3Institute of Human Morphology, Tsyrupa st. 3, 117418 Moscow, Russia

Tóm tắt

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.

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