Regulation of the Migration and Survival of Monocyte Subsets by Chemokine Receptors and Its Relevance to Atherosclerosis
Open accessAbstract
Monocytes are central mediators in the advance of atherosclerotic plaque, making them a natural therapeutic target for reducing disease burden. Here, we highlight recent advances in our current understanding of monocyte heterogeneity and its relevance to regulation of monocyte accumulation and function within atherosclerotic plaques. Differences that distinguish monocyte subsets include differential expression of chemokine receptors, especially CCR2 and CX3CR1. Ablation of expression of these 2 receptors (or their ligands) in mice has an additive inhibition on monocyte recruitment to atherosclerotic plaques. Moreover, simultaneously interfering with 3 key pathways—CCR2, CX3CR1, and CCR5—essentially abolishes atherosclerosis in mice. Here, we discuss how these chemokine receptors act at multiple points on at least 1 monocyte subset, regulating their mobilization from bone marrow, survival, or recruitment to plaques. Finally, we discuss how this knowledge may be useful clinically, emphasizing that CX3CR1 may in particular be a viable target for therapeutic manipulation of monocyte-derived cell fate in cardiovascular disease.
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In atherosclerotic mice, intimal infiltrating macrophages derive from circulating pro-inflammatory classical Ly6Chigh monocytes.
“In atherosclerotic mice, these infiltrating macrophages are derived from circulating pro-inflammatory, classical Ly6Chigh monocytes148.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [148]
In humans, intimal macrophages derive from classical CD14+CD16- monocytes, which are the predominant blood monocytes and are preferentially recruited to inflammatory sites including atherosclerotic plaques.
“In humans, the macrophages in the arterial intima derive from the classical CD14+CD16- monocytes, which predominate in the circulating blood and are preferentially recruited into inflammatory sites, including the atherosclerotic plaques148.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [148]
Monocytes become macrophages with different phenotypes according to the combinations and ratios of growth factors, chemokines and cytokines present.
“In the arterial intima, as in other tissues, monocytes differentiate into macrophages with different phenotypes depending on the presence of growth factors, chemokines and cytokines in various combinations and ratios148.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [148]
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Deleterious Genetic Influence of CX3CR1 Genotypes on HIV-1 Disease Progression
Faure, S., Meyer, L., Génin, E., et al. (2003) · JAIDS Journal of Acquired Immune Deficiency Syndromes · doi:10.1097/00126334-200303010-00014 · Cited by 34 · see citing works
Qu, C., Moran, T. M., & Randolph, G. J. (2003) · The Journal of Immunology · doi:10.4049/jimmunol.170.2.1010 · Cited by 21 · see citing works
Self-citationA CX 3 CR1 Genotype Associated with Retinal Vasculitis in Patients in the United Kingdom
Wallace, G. R., Vaughan, R. W., Kondeatis, E., Mathew, R. G., Chen, Y., GRAHAM, E. M., & Stanford, M. R. (2006) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.05-1631 · Cited by 14 · see citing works
Epstein-Barr virus-dependent lymphoproliferative disease: critical role of IL-6
(2000) · Pure Amsterdam UMC · doi:10.1002/1521-4141(200007)30:7 · Cited by 1 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Monocyte recruitment during infection and inflammation
Shi, C., & Pamer, E. G. (2011) · Nature Reviews Immunology · doi:10.1038/nri3070 · Cited by 3,015 · see citing works
Gleeson, M., Bishop, N. C., Stensel, D. J., Lindley, M. R., Mastana, S. S., & Nimmo, M. A. (2011) · Nature Reviews Immunology · doi:10.1038/nri3041 · Cited by 2,470 · see citing works
From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation
Italiani, P., & Boraschi, D. (2014) · Frontiers in Immunology · doi:10.3389/fimmu.2014.00514 · Cited by 2,067 · see citing works
Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities
Bäck, M., Yurdagul, A., Tabas, I., Öörni, K., & Kovanen, P. T. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0169-2 · Cited by 1,341 · see citing works
Monocyte differentiation and antigen-presenting functions
Jakubzick, C. V., Randolph, G. J., & Henson, P. M. (2017) · Nature Reviews Immunology · doi:10.1038/nri.2017.28 · Cited by 910 · see citing works
Self-citationSeidler, S., Zimmermann, H. W., Bartneck, M., Trautwein, C., & Tacke, F. (2010) · BMC Immunology · doi:10.1186/1471-2172-11-30 · Cited by 390 · see citing works
Cardilo‐Reis, L., Gruber, S., Schreier, S. M., Drechsler, M., Papac‐Milicevic, N., Weber, C., Wagner, O., Stangl, H., Soehnlein, O., & Binder, C. J. (2012) · EMBO Molecular Medicine · doi:10.1002/emmm.201201374 · Cited by 292 · see citing works
Schiopu, A., Bengtsson, E., Gonçalves, I., Nilsson, J., Fredrikson, G. N., & Björkbacka, H. (2016) · Journal of the American Heart Association · doi:10.1161/jaha.115.002851 · Cited by 25 · see citing works
Baba, O., Horie, T., Nakao, T., Hakuno, D., Nakashima, Y., Nishi, H., Kuwabara, Y., Nishiga, M., Nishino, T., Ide, Y., et al. (2018) · Molecular and Cellular Biology · doi:10.1128/mcb.00604-17 · Cited by 12 · see citing works
- Authors
- Gautier, E. L., Jakubzick, C., & Randolph, G. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2009-10
- Volume
- 29
- Issue
- 10
- Pages
- 1412-1418
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC2782657
- OpenAlex
- W2123811618
- Cited by
- 216
- References
- 91
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 2 · 2023: 11 · 2022: 7 · 2021: 6 · 2020: 10 · 2019: 8 · 2018: 8 · 2017: 17 · 2016: 13 · 2015: 15 · 2014: 18 · 2013: 23 · 2012: 26
- FWCI
- 1.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL084312, HL-084312)
- National Institute of Allergy and Infectious Diseases (AI049653, AI061741, R01AI049653, R01AI061741, R37AI049653)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- monocytes, atherosclerosis, chemokine receptors, CCR2, CX3CR1, CCR5, monocyte heterogeneity, monocyte recruitment, monocyte survival, monocyte mobilization, atherosclerotic plaque, therapeutic target
- MeSH terms
- CX3C Chemokine Receptor 1, Chemokine CXCL16, Animals, Cell Movement, Cell Survival, Humans, Monocytes, Receptors, Chemokine, Chemokines, CXC, Atherosclerosis, Receptors, Scavenger, Receptors, Oxidized LDL, Receptors, CCR2
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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