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Leukocyte Influx in Atherosclerosis
Abstract
Atherosclerosis is a chronic inflammatory disease of the arterial wall and an increasing body of evidence suggests that the immune system actively participates in the initiation, progression and persistence of atherosclerosis. Different types of leukocytes such as T and B lymphocytes, natural killer cells (NK) and NKT cells, macrophages, dendritic cells and mast cells have been found within atherosclerosis-prone aortas. The mechanisms of monocyte recruitment have been partially characterized and involve P-selectin, E-selectin, VCAM-1, ICAM-1 and JAM-A. CXCL1, CCL5, CXCL4, CXCL7 and MIF are also implicated in monocyte trafficking into aortas. Recently it has been reported that Ly6C(high) and Ly6C(low) monocyte subsets differently use CCL2, CX3CL1 and CCL5 for their homing into atherosclerotic aortas. T and B lymphocytes constitutively migrate into the normal and atherosclerotic aortic wall in an L-selectin-dependent manner. Recent studies suggest an important role of CCL5, CXCL10, CXCL16, CXCR6 and MIF in T cell influx into the atherosclerotic wall. However, there is little information available on the mechanisms of recruitment of other types of the immune cells such as NK, NKT and mast cells. In this review we shall summarize what is known about leukocyte recruitment into the aortic wall during atherosclerosis with a focus on mouse model systems.
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“Briefly, in atherosclerosis, circulating monocytes are recruited to sites of fatty deposit accumulation within the vascular intima and subintima via CCR2 and endothelial adhesion mediated mechanisms [49–52].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [49]
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Metadata
- Authors
- Galkina, E., & Ley, K.
- Affiliations
- University of Virginia (US)
- Venue
- Current Drug Targets
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2007-12-01
- Volume
- 8
- Issue
- 12
- Pages
- 1239-1248
- ISSN
- 1389-4501 (ISSN-L)
- OpenAlex
- W2079678457
- Cited by
- 118
- References
- 0
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 1 · 2022: 8 · 2021: 3 · 2020: 5 · 2019: 3 · 2018: 7 · 2017: 5 · 2016: 7 · 2015: 9 · 2014: 8 · 2013: 10 · 2012: 14
- FWCI
- 2.85
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Drug Targets (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL055798, HL-55798, HL 58108, R01HL058108)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- atherosclerosis, leukocyte recruitment, monocyte trafficking, T cell migration, B cells, natural killer cells, NKT cells, macrophages, dendritic cells, mast cells, chemokines, adhesion molecules, P-selectin, E-selectin, VCAM-1, ICAM-1, JAM-A, RANTES, CXCL10, CXCL16, CXCR6, macrophage migration inhibitory factor, L-selectin, aortitis, mouse model
- MeSH terms
- Animals, Aorta, Disease Models, Animal, Leukocytes, Chemokines, Receptors, Chemokine, Atherosclerosis, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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