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Nat Immunol. 2014 Oct;15(10):929-937. doi: 10.1038/ni.2967. Epub 2014 Aug 24.

Constant replenishment from circulating monocytes maintains the macrophage pool in the intestine of adult mice.

Author information

1
Institute of Infection, Immunity and Inflammation, College of Veterinary, Medical and Life Science, University of Glasgow, G12 8TA, Scotland, UK.
2
Centre for Molecular and Cellular Biology of Inflammation (CMCBI), New Hunt's House, King's College London, Great Maze Pond, London SE1 1UL, UK.
3
Peter Gorer Department of Immunobiology, King's College London, London SE1 9RT, UK.
4
Centre d'Immunologie de Marseille-Luminy (CIML), Aix Marseille Universite, Marseille, France.
5
INSERM U1104, Marseille, France.
6
CNRS UMR7280, Marseille, France.
7
Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
8
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
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Contributed equally

Erratum in

  • Nat Immunol. 2014 Nov;15(11):1090.

Abstract

The paradigm that macrophages that reside in steady-state tissues are derived from embryonic precursors has never been investigated in the intestine, which contains the largest pool of macrophages. Using fate-mapping models and monocytopenic mice, together with bone marrow chimera and parabiotic models, we found that embryonic precursor cells seeded the intestinal mucosa and demonstrated extensive in situ proliferation during the neonatal period. However, these cells did not persist in the intestine of adult mice. Instead, they were replaced around the time of weaning by the chemokine receptor CCR2-dependent influx of Ly6C(hi) monocytes that differentiated locally into mature, anti-inflammatory macrophages. This process was driven largely by the microbiota and had to be continued throughout adult life to maintain a normal intestinal macrophage pool.

PMID:
25151491
PMCID:
PMC4169290
DOI:
10.1038/ni.2967
[Indexed for MEDLINE]
Free PMC Article

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