Monocyte subsets differentially employ CCR2, CCR5, and CX3CR1 to accumulate within atherosclerotic plaques
Open accessAbstract
Monocytes participate critically in atherosclerosis. There are 2 major subsets expressing different chemokine receptor patterns: CCR2(+)CX3CR1(+)Ly-6C(hi) and CCR2(-)CX3CR1(++)Ly-6C(lo) monocytes. Both C-C motif chemokine receptor 2 (CCR2) and C-X(3)-C motif chemokine receptor 1 (CX3CR1) are linked to progression of atherosclerotic plaques. Here, we analyzed mouse monocyte subsets in apoE-deficient mice and traced their differentiation and chemokine receptor usage as they accumulated within atherosclerotic plaques. Blood monocyte counts were elevated in apoE(-/-) mice and skewed toward an increased frequency of CCR2(+)Ly-6C(hi) monocytes in apoE(-/-) mice fed a high-fat diet. CCR2(+)Ly-6C(hi) monocytes efficiently accumulated in plaques, whereas CCR2(-)Ly-6C(lo) monocytes entered less frequently but were more prone to developing into plaque cells expressing the dendritic cell-associated marker CD11c, indicating that phagocyte heterogeneity in plaques is linked to distinct types of entering monocytes. CCR2(-) monocytes did not rely on CX3CR1 to enter plaques. Instead, they were partially dependent upon CCR5, which they selectively upregulated in apoE(-/-) mice. By comparison, CCR2(+)Ly-6C(hi) monocytes unexpectedly required CX3CR1 in addition to CCR2 and CCR5 to accumulate within plaques. In many other inflammatory settings, these monocytes utilize CCR2, but not CX3CR1, for trafficking. Thus, antagonizing CX3CR1 may be effective therapeutically in ameliorating CCR2(+) monocyte recruitment to plaques without impairing their CCR2-dependent responses to inflammation overall.
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In atherosclerosis, circulating monocytes are recruited to fatty deposits in vascular intima/subintima via CCR2 and endothelial adhesion mechanisms.
“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 [52]
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- Authors
- Tacke, F., Alvarez, D., Kaplan, T. J., Jakubzick, C., Spanbroek, R., Llodra, J., Garin, A., Liu, J., Mack, M., van Rooijen, N., Lira, S. A., Habenicht, A. J., & Randolph, G. J.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Friedrich Schiller University Jena (DE)
- Erasmus MC Transplant Institute (NL)
- University of Regensburg (DE)
- Corresponding author
- Randolph, Gwendalyn J.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2007-01-02
- Volume
- 117
- Issue
- 1
- Pages
- 185-194
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1716202
- OpenAlex
- W2052554962
- Cited by
- 1,323
- References
- 8
- Citations by year
- 2026: 21 · 2025: 30 · 2024: 64 · 2023: 70 · 2022: 56 · 2021: 61 · 2020: 62 · 2019: 64 · 2018: 79 · 2017: 75 · 2016: 88 · 2015: 90 · 2014: 75 · 2013: 91 · 2012: 96
- FWCI
- 27.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- University of Regensburg Publication Server (University of Regensburg) (acceptedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- National Institutes of Health (HL69446, AI49653)
- Canadian Institutes of Health Research
- National Heart, Lung, and Blood Institute (HL69446, R01HL069446)
- National Institute of Allergy and Infectious Diseases (AI49653, R01AI049653)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 067381, R01DK067381)
- 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
- monocyte subsets, atherosclerosis, atherosclerotic plaque, CCR2, CCR5, CX3CR1, chemokine receptors, Ly6C, monocyte recruitment, ApoE-deficient mice, high-fat diet, CD11c, monocyte differentiation
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Monocytes, Receptors, Chemokine, Receptors, CCR5, Models, Animal, Atherosclerosis, Mice, 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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