Nonclassical Patrolling Monocyte Function in the Vasculature
Open accessAbstract
Nonclassical patrolling monocytes are characterized by their unique ability to actively patrol the vascular endothelium under homeostatic and inflammatory conditions. Patrolling monocyte subsets (CX3CR1 high Ly6C − in mouse and CX3CR1 high CD14 dim CD16 + in humans) are distinct from the classical monocyte subsets (CCR2 high Ly6C + in mouse and CCR2 high CD14 + CD16 − in humans) and exhibit unique functions in the vasculature and inflammatory disease. Patrolling monocytes function in several disease settings to remove damaged cells and debris from the vasculature and have been associated with wound healing and the resolution of inflammation in damaged tissues. This review highlights the unique functions of these patrolling monocytes in the vasculature and during inflammation.
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Non-classical monocytes are known as patrolling monocytes, named for their role in surveilling the vasculature and crossing the blood brain barrier to remove damaged tissue, including amyloid plaques.
“Non-classical monocytes are known as patrolling monocytes, named for their role in surveilling the vasculature and crossing the blood brain barrier to remove damaged tissue, including amyloid plaques.39–41”
From TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice (2025) · cites this paper as [41]
The Introduction identifies nonclassical monocytes as patrolling cells, and “Neurological diseases and damage” says they patrol brain vasculature and remove amyloid beta from it. That section does not say they cross the blood-brain barrier to remove damaged tissue or amyloid plaques; it instead describes the barrier as maintained by perivascular macrophages. (LLM, conf=0.88)
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- Authors
- Thomas, G., Tacke, R., Hedrick, C. C., & Hanna, R. N.
- Affiliations
- La Jolla Institute for Immunology (US)
- Corresponding author
- Hanna, Richard N.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2015-06
- Volume
- 35
- Issue
- 6
- Pages
- 1306-1316
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC4441550
- OpenAlex
- W2127385800
- Cited by
- 367
- References
- 98
- Citations by year
- 2026: 31 · 2025: 35 · 2024: 32 · 2023: 33 · 2022: 40 · 2021: 43 · 2020: 29 · 2019: 31 · 2018: 26 · 2017: 38 · 2016: 25 · 2015: 4
- FWCI
- 15.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL118765, P01HL055798)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- non-classical monocytes, CX3CR1, Ly6C, CD14, CD16, CCR2, classical monocytes, vascular endothelium, inflammation, wound healing, inflammation resolution, monocyte subsets
- MeSH terms
- Animals, Arthritis, Cardiovascular Diseases, Cell Adhesion, Cell Differentiation, Cell Survival, Endothelium, Vascular, Humans, Inflammation, Kidney Diseases, Lupus Erythematosus, Systemic, Monocytes, Nervous System Diseases, Mice
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