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Monocyte-Macrophages and T Cells in Atherosclerosis
Open accessAbstract
Atherosclerosis is an arterial disease process characterized by the focal subendothelial accumulation of apolipoprotein-B-containing 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 and can lead to arterial damage and thrombosis-induced organ infarction. The innate immune response is regulated at various stages, from hematopoiesis to monocyte changes and macrophage activation. The adaptive immune response is regulated primarily by mechanisms that affect the balance between regulatory and effector T cells. Mechanisms related to cellular cholesterol, phenotypic plasticity, metabolism, and aging play key roles in affecting these responses. Herein, we review select topics that shed light on these processes and suggest new treatment strategies.
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“Immunosuppressive drug regimens may have adverse effects on lipid metabolism leading to increases in TC, VLDL, and TGs, and in the size and density of LDL particles.”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [502]
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“These effects vary with different immunosuppressive drugs [497,498,502-506].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [502]
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Metadata
- Authors
- Tabas, I., & Lichtman, A. H.
- Affiliations
- Columbia University Irving Medical Center (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Tabas, Ira
- Lichtman, Andrew H.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 47
- Issue
- 4
- Pages
- 621-634
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC5747297
- OpenAlex
- W2766451938
- Cited by
- 646
- References
- 155
- Citations by year
- 2026: 53 · 2025: 57 · 2024: 72 · 2023: 65 · 2022: 86 · 2021: 102 · 2020: 80 · 2019: 78 · 2018: 49 · 2017: 4
- FWCI
- 6.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (R01 HL132412, HL127464, HL075662, P01 HL087123, R01 HL087282, HL131862)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- atherosclerosis, monocytes/macrophages, T cells, innate immune response, adaptive immune response, damage-associated molecular patterns, apolipoprotein B-containing lipoproteins, macrophage activation, regulatory T cells, effector T cells, chronic inflammation, thrombosis, hematopoiesis, cholesterol, phenotypic plasticity, aging, atherosclerosis treatment
- MeSH terms
- Animals, Humans, Immunity, Innate, Lipoproteins, Macrophages, Monocytes, T-Lymphocytes, Models, Immunological, Atherosclerosis, Adaptive Immunity
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