Cited by 422Chemokine receptors and signalingImmune cells in cancerImmune Response and Inflammation

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CX3CR1+ CD115+ CD135+ common macrophage/DC precursors and the role of CX3CR1 in their response to inflammation

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Auffray, Cedric, Fogg, Darin K., Narni-Mancinelli, Emilie, Senechal, Brigitte, Trouillet, Celine, Saederup, Noah, Leemput, Julia, Bigot, Karine, Campisi, Laura, Abitbol, Marc, Molina, Thierry, Charo, Israel, Hume, David A., Cumano, Ana, Lauvau, Gregoire, Geissmann, Frederic·2009·Journal of Experimental Medicine

DOI 10.1084/jem.20081385PMC PMC2699130

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Abstract

CX3CR1 expression is associated with the commitment of CSF-1R+ myeloid precursors to the macrophage/dendritic cell (DC) lineage. However, the relationship of the CSF-1R+ CX3CR1+ macrophage/DC precursor (MDP) with other DC precursors and the role of CX3CR1 in macrophage and DC development remain unclear. We show that MDPs give rise to conventional DCs (cDCs), plasmacytoid DCs (PDCs), and monocytes, including Gr1+ inflammatory monocytes that differentiate into TipDCs during infection. CX3CR1 deficiency selectively impairs the recruitment of blood Gr1+ monocytes in the spleen after transfer and during acute Listeria monocytogenes infection but does not affect the development of monocytes, cDCs, and PDCs.

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Additional file 3 of Phenotypic and functional alterations of monocyte subsets with aging
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Additional file 1 of Phenotypic and functional alterations of monocyte subsets with aging
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Additional file 2 of Phenotypic and functional alterations of monocyte subsets with aging
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Authors: Auffray, C., Fogg, D. K., Narni-Mancinelli, E., Senechal, B., Trouillet, C., Saederup, N., Leemput, J., Bigot, K., Campisi, L., Abitbol, M., Molina, T., Charo, I., Hume, D. A., Cumano, A., Lauvau, G., & Geissmann, F.
Affiliations: Laboratory of Biology of the Mononuclear Phagocyte System, Institut National de la Santé et de la Recherche Médicale (INSERM) U838, Université Paris-Descartes, 75015 Paris, France 1
Inserm (FR)
INSERM U924, Université de Nice-Sophia Antipolis, 06560 Valbonne, France 2
University of California, San Francisco (US)
Université Paris Descartes (FR)
Roslin Institute (GB)
ORCID: Leemput, Julia
Campisi, Laura
Abitbol, Marc
Molina, Thierry
Hume, David A.
Cumano, Ana
Lauvau, Gregoire
Venue: Journal of Experimental Medicine
Publisher: Rockefeller University Press
Published: 2009-03-09
Volume: 206
Issue: 3
Pages: 595-606
ISSN: 0022-1007 (ISSN-L)
1540-9538
DOI: 10.1084/jem.20081385
PMC: PMC2699130
OpenAlex: W2142750845
Cited by: 422
References: 50
Citations by year: 2026: 4 · 2025: 7 · 2024: 14 · 2023: 17 · 2022: 16 · 2021: 21 · 2020: 17 · 2019: 26 · 2018: 21 · 2017: 28 · 2016: 32 · 2015: 24 · 2014: 33 · 2013: 43 · 2012: 36
FWCI: 19.67
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: The Journal of Experimental Medicine (publishedVersion)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
HAL (submittedVersion, other-oa)
Research Portal (King's College London) (submittedVersion)
Topics: Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: CX3CR1, CSF1R, myeloid dendritic cells, plasmacytoid dendritic cells, monocytes, Listeria monocytogenes infection, monocyte recruitment, spleen, inflammation, myeloid development
MeSH terms: CX3C Chemokine Receptor 1, Animals, Bone Marrow Cells, Cell Differentiation, Cell Movement, Cell Survival, Dendritic Cells, Inflammation, Listeriosis, Listeria monocytogenes, Macrophages, Monocytes, Phenotype, Spleen, Stem Cells, Tumor Necrosis Factor-alpha, Receptor, Macrophage Colony-Stimulating Factor, Reactive Oxygen Species, Receptors, Chemokine, Cell Proliferation, Mice, fms-Like Tyrosine Kinase 3, Nitric Oxide Synthase Type II

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CX3CR1+ CD115+ CD135+ common macrophage/DC precursors and the role of CX3CR1 in their response to inflammation

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