Monocyte-Macrophages and T Cells in Atherosclerosis

By I. Tabas, A. Lichtman. Immunity, 2017

595 citations recorded by the source corpus.

Atherosclerosis is an arterial disease process characterized by the focal subendothelial accumulation of apolipoprotein B-lipoproteins, immune and vascular wall cells, and extracellular matrix. The lipoproteins acquire features of damage-associated molecular patterns and trigger first an innate immune response, dominated by monocyte-macrophages, and then an adaptive immune response. These inflammatory responses often become chronic and non-resolving, leading to arterial damage and thrombosis-induced organ infarction. The innate immune response is regulated at various stages, from hematopoiesis through monocyte changes and macrophage activation. The adaptive immune response is regulated primarily by mechanisms that affect the balance of regulatory vs. effector T cells. Mechanisms related to cellular cholesterol, phenotypic plasticity, metabolism, and aging play key roles in regulating these responses. Herein we review select topics that shed light on these processes and suggest new treatment strategies.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/5ce3940f372c31362f2dd3c5bc3fbb50a31b0644

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Citations in the corpus

2019 ESC/EAS guidelines for the management of dyslipidaemias: Lipid modification to reduce cardiovascular risk. (2019, background): “Almost all cell types of the immuno-inflammatory system, such as macrophages, and T- and B-cells, as well as many pro- and anti-inflammatory cytokines and chemokines, have been identified during the process of atherosclerosis.(526) Interestingly, cholesterol accumulation in cells triggers the inflam”
Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel (2020, background): “Very low-density lipoprotein 1 remodelling gives rise to remnants within the VLDL size range that are enriched in apoE; such circulating remnants can be removed by several mechanisms, primarily in the liver, including the LDL receptor-related protein, heparan sulfate proteoglycans, and LDL receptor.”
Diversity, Mechanisms and Significance of Macrophage Plasticity (2019, background): “Macrophage adaptability underlies their role in atherosclerosis and cardiovascular pathology (19; 20; 104; 105), neurodegeneration (18), autoimmunity and autoinflammation (e.”