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Tissue-Resident Macrophages Self-Maintain Locally throughout Adult Life with Minimal Contribution from Circulating Monocytes
Open accessAbstract
Despite accumulating evidence suggesting local self-maintenance of tissue macrophages in the steady state, the dogma remains that tissue macrophages derive from monocytes. Using parabiosis and fate-mapping approaches, we confirmed that monocytes do not show significant contribution to tissue macrophages in the steady state. Similarly, we found that after depletion of lung macrophages, the majority of repopulation occurred by stochastic cellular proliferation in situ in a macrophage colony-stimulating factor (M-Csf)- and granulocyte macrophage (GM)-CSF-dependent manner but independently of interleukin-4. We also found that after bone marrow transplantation, host macrophages retained the capacity to expand when the development of donor macrophages was compromised. Expansion of host macrophages was functional and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-deficient progenitors. Collectively, these results indicate that tissue-resident macrophages and circulating monocytes should be classified as mononuclear phagocyte lineages that are independently maintained in the steady state.
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“Our findings are consistent with reports that macrophage progenitors develop from the primitive ectoderm of the yolk sac4 and give rise to tissue macrophages that do not have a monocytic progenitor16,17.”
From Identification of a unique TGF-β–dependent molecular and functional signature in microglia (2014) · cites this paper as [16]
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“In addition, the normal arterial intima of mice and humans, like any tissue of the mammalian body, contains tissue-resident macrophages, which arise from embryonic precursors and from bone-marrow-derived circulating monocytes immediately after birth144.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [144]
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“These macrophages self-renew and fulfil homeostatic and physiological functions in the tissue concerned144.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [144]
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“9c; Supplementary Movies 3 – 4) and ingestion of zymosan did not alter mitochondrial size signi fi cantly (Fig.”
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Self-citationDevelopment and function of tissue resident macrophages in mice
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Microglia in Alzheimer’s disease: A target for immunotherapy
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Teaching Old Dogs New Tricks? The Plasticity of Lung Alveolar Macrophage Subsets
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“Similar patterns of AM depletion and proliferation in situwere observed with poly I:C and clodronate liposome administration [3], confirming the ability of resident macrophages to expand in inflammatory settings.”
BackgroundResultInfluentialMicroglia as Central Protagonists in the Chronic Stress Response
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“Along with the fact that CFU-M were generated at low frequency from peripheral blood (Figure 1A), this provided initial evidence that the cells responsible for arterial macrophage colonies are not monocytes, consistent with recent data showing the nonmonocyte origins of tissue-resident macrophages.(9,11,12) This was s…”
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Non-alcoholic steatohepatitis induces transient changes within the liver macrophage pool
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Functional regulation of decidual macrophages during pregnancy
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Origins and diversity of macrophages in health and disease
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Thyroid hormone metabolism in innate immune cells
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Bhlhe40 and Bhlhe41 Transcription Factors Regulate Alveolar Macrophage Self‐renewal and Identity
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Self-citationThe Interplay of HIV-1 and Macrophages in Viral Persistence
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Macrophages: Gatekeepers of Tissue Integrity
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Impact on the brain of the inflammatory response to surgery
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“The resident immunocompentent macrophage population is long-lived and is not replenished by myeloid-derived cells but may self-renew [46].”
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The macrophage: a key player in the pathophysiology of peripheral neuropathies
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Resident tissue macrophages: Key coordinators of tissue homeostasis beyond immunity
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“After the groundbreaking finding that RTMs can originate from extra-embryonic yolk sac progenitors and populate tissues from the early stages of embryogenesis ( 14 – 16 ), there has been resurged enthusiasm for investigating the contribution of RTMs to tissue homeostasis.”
Background
Metadata
- Authors
- Hashimoto, D., Chow, A., Noizat, C., Teo, P., Beasley, M. B., Leboeuf, M., Becker, C. D., See, P., Price, J., Lucas, D., Greter, M., Mortha, A., Boyer, S. W., Forsberg, E. C., Tanaka, M., van Rooijen, N., García-Sastre, A., Stanley, E. R., Ginhoux, F., Frenette, P. S., & Merad, M.
- Affiliations
- Tisch Cancer Institute (US)
- Albert Einstein College of Medicine (US)
- Agency for Science, Technology and Research (SG)
- Icahn School of Medicine at Mount Sinai (US)
- University of Zurich (CH)
- University of California, Santa Cruz (US)
- Tokyo University of Pharmacy and Life Sciences (JP)
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 38
- Issue
- 4
- Pages
- 792-804
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3853406
- OpenAlex
- W1973433801
- Cited by
- 2,311
- References
- 49
- Citations by year
- 2026: 132 · 2025: 151 · 2024: 158 · 2023: 168 · 2022: 204 · 2021: 211 · 2020: 219 · 2019: 185 · 2018: 179 · 2017: 188 · 2016: 152 · 2015: 155 · 2014: 148 · 2013: 47
- FWCI
- 92.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- California Institute for Regenerative Medicine
- California Institute of Regenerative Medicine
- National Institutes of Health
- Japan Society for the Promotion of Science (23390095)
- National Heart, Lung, and Blood Institute (HL097700, HL069438, R01HL116340, R01HL086899, R01HL097700, F30HL099028, R01HL069438, HL116340)
- National Cancer Institute (CA154947A, R01CA173861, R01CA154947)
- National Institute of General Medical Sciences (T32GM008646)
- National Institute of Allergy and Infectious Diseases (AI 089987, U19AI089987, AI10008)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK056638, DK056638)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- tissue-resident macrophages, macrophage self-renewal, monocytes, lung macrophages, macrophage colony-stimulating factor, GM-CSF, IL-4, pulmonary alveolar proteinosis, bone marrow transplantation, parabiosis, fate mapping
- MeSH terms
- Adult, Animals, Cell Survival, Cells, Cultured, Homeostasis, Humans, Lung, Macrophages, Mice, Mutant Strains, Parabiosis, Interleukin-4, Bone Marrow Transplantation, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, Knockout, Cell Proliferation, Mice
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