Cited by 5,175Neuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanismsMultiple Sclerosis Research Studies

Fate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages

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Ginhoux, Florent, Greter, Melanie, Leboeuf, Marylene, Nandi, Sayan, See, Peter, Gokhan, Solen, Mehler, Mark F., Conway, Simon J. +4 more·2010·Science

Abstract

Primitive Origins for Microglia: Microglia are the resident macrophages of the central nervous system and are associated with neurodegeneration and brain inflammatory diseases. Although the developmental origins of other tissue macrophage populations are well established, the origins of microglia remain controversial. Ginhoux et al. (p. 841 , published online 21 October) used in vivo lineage tracing studies to show that microglia arise early in mouse development and derive from primitive macrophages in the yolk sac. This is in contrast to other cells of the mononuclear phagocyte system, which arise later in development from a distinct progenitor population.

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Crossref · 10.1126/science.1194637

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31 of 31 references verified0 citation errors · 0 not checkable

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Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • CD11b+ CD45+ cells are absent from non-engrafted CSF1R knockout brains.

    “Two weeks after injection, CSF1R knockout brains had been partially repopulated with CD11b+ CD45+ cells (Fig. S7B), which are absent from non-engrafted brains (Ginhoux et al., 2010).”

    From Diverse Requirements for Microglial Survival, Specification, and Function Revealed by Defined-Medium Cultures (2017) · cites this paper as Ginhoux et al., 2010

    The CSF-1R results passage (labelled Abstract; page unavailable) says microglia are largely absent throughout life in CSF-1R–deficient mice and absent in adults lacking the receptor. An earlier passage identifies developing-brain myeloid cells by CD11b and CD45, but the paper does not establish that all CD11b+ CD45+ cells are absent from non-engrafted knockout brains. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • Microglia originate from the yolk sac during early embryonic development, whereas peripheral macrophages originate from hematopoietic stem cells in the bone marrow.

    “Importantly, microglia originate from the yolk sac during early embryonic development, whereas peripheral macrophages originate from hematopoietic stem cells in the bone marrow (19).”

    From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [19]

    The paper’s Abstract and developmental discussion support a yolk-sac origin for microglia from primitive myeloid progenitors early in mouse embryogenesis. The developmental discussion says adult tissue macrophages are *thought* to derive from bone-marrow monocytes; it does not establish that peripheral macrophages generally originate from bone-marrow hematopoietic stem cells. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Microglia are uniformly CX3CR1+ from early embryonic time points through adulthood.

    “microglia are uniformly CX3CR1+ from early embryonic time points through adulthood (Cardona et al., 2006; Ginhoux et al., 2010; Schulz et al., 2012)”

    From Differential roles of microglia and monocytes in the inflamed central nervous system (2014) · cites this paper as Ginhoux et al., 2010

    The passage on developmental markers (section labeled Abstract; page unavailable) identifies CX3CR1 as a microglial marker and reports CX3CR1-expressing myeloid cells in the developing brain from E9.5. It does not establish that all microglia express CX3CR1 uniformly at every stage through adulthood. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Microglia arise from yolk sac erythromyeloid precursors and migrate into the brain parenchyma during early development.

    “It is believed that microglia arise from yolk sac erythromyeloid precursors and migrate into the brain parenchyma during early development [43,44,45].”

    From The Cuprizone Model: Dos and Do Nots (2020) · cites this paper as [44]

    The paper reports that adult microglia derive from primitive myeloid progenitors in the yolk sac and that Runx1+ progenitors migrate into the developing brain between E8.5 and E9.5 (Abstract; page unavailable). It does not identify those progenitors specifically as erythromyeloid precursors, so that part of the claim is more specific than the source supports. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Microglia share much of their genetic make-up, complement of proteins, and function, with other immune cells, particularly macrophages.

    “Microglia share much of their genetic make-up, complement of proteins, and function, with other immune cells, particularly macrophages [129]”

    From TREM2/PLCγ2 signalling in immune cells: function, structural insight, and potential therapeutic modulation (2021) · cites this paper as [129]

    The paper’s Abstract describes microglia as resident macrophages of the CNS, and the body text reports that embryonic microglia resemble yolk sac macrophages in phenotype and express similar amounts of CSF-1R. These passages support a macrophage relationship and some shared characteristics, but they do not establish the claimed broad similarity in genetic make-up, protein complement, and function across other immune cells. Page numbers are unavailable in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

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  1. [4]Ling EA J. Anat 1979 128 847 489472 PMC1232886

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Authors
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., Samokhvalov, I. M., & Merad, M.
Affiliations
  • Singapore Immunology Network (SG)
  • Icahn School of Medicine at Mount Sinai (US)
  • Department of Gene and Cell Medicine and the Immunology Institute, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA.
  • Albert Einstein College of Medicine (US)
  • Institute for Brain Disorders and Neural Regeneration, Rose F. Kennedy Center for Research on Intellectual and Developmental Disabilities, and Department of Neurology, Albert Einstein College of Medicine, 1410 Pelham Parkway South, Bronx, NY 10461, USA.
  • Indiana University Indianapolis (US)
  • RIKEN (JP)
Corresponding author
Ginhoux, Florent
Venue
Science
Published
2010-11-05
Volume
330
Issue
6005
Pages
841-845
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2148898943
Cited by
5,175
References
32
Citations by year
2026: 286 · 2025: 360 · 2024: 447 · 2023: 369 · 2022: 443 · 2021: 483 · 2020: 425 · 2019: 382 · 2018: 363 · 2017: 328 · 2016: 279 · 2015: 279 · 2014: 271 · 2013: 219 · 2012: 137
FWCI
87.47
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • IUScholarWorks (Indiana University) (submittedVersion)
Funders
  • National Science Foundation
  • National Institutes of Health (CA26504)
  • RIKEN
  • National Heart, Lung, and Blood Institute (HL086899, R01HL086899, R01HL060714)
  • National Institute of Mental Health (R01MH066290, MH66290)
  • National Cancer Institute (CA-32551, R01CA032551, R37CA026504, R01CA112100, CA26504, CA112100, R01CA026504)
  • National Institute of Allergy and Infectious Diseases (AI080884, R01AI080884)
  • National Institute of Neurological Disorders and Stroke (NS38902, R01NS038902)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
Keywords
myeloid progenitor cells, CSF-1, CSF-1 receptor, reticuloendothelial system, hematopoietic progenitor cells, lineage tracing, neuroinflammation, neurodegenerative diseases
MeSH terms
Animals, Brain, Cell Differentiation, Embryo, Mammalian, Female, Hematopoiesis, Hematopoietic Stem Cells, Homeostasis, Macrophages, Mice, Inbred C57BL, Yolk Sac, Macrophage Colony-Stimulating Factor, Receptor, Macrophage Colony-Stimulating Factor, Microglia, Cell Lineage, Myeloid Progenitor Cells, Cell Proliferation, Core Binding Factor Alpha 2 Subunit, Mice, Gene Knock-In Techniques

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