Protective and pathogenic functions of macrophage subsets
Open accessAbstract
Macrophages are strategically located throughout the body tissues, where they ingest and process foreign materials, dead cells and debris and recruit additional macrophages in response to inflammatory signals. They are highly heterogeneous cells that can rapidly change their function in response to local microenvironmental signals. In this Review, we discuss the four stages of orderly inflammation mediated by macrophages: recruitment to tissues; differentiation and activation in situ; conversion to suppressive cells; and restoration of tissue homeostasis. We also discuss the protective and pathogenic functions of the various macrophage subsets in antimicrobial defence, antitumour immune responses, metabolism and obesity, allergy and asthma, tumorigenesis, autoimmunity, atherosclerosis, fibrosis and wound healing. Finally, we briefly discuss the characterization of macrophage heterogeneity in humans.
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The in vitro liver system maintained differentiated cell types, as shown by CD68 and reelin expression in macrophages and hepatic stellate cells and E-cadherin in hepatocytes.
“CD68 and reelin, markers for MΦs and HSCs, respectively (12,13), were expressed in our system at the end of the experiment, reflecting the maintenance of the cell types in a differentiated state.”
From Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis (2016) · cites this paper as [13]
Macrophage polarization and plasticity play important roles in a diverse spectrum of disease processes.
“Macrophage polarization and plasticity have been shown to play important roles in a diverse spectrum of disease processes [32,33].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [32]
Prolonged inflammation and remodeling can lead to fibrosis or hypertrophic scar formation due to dysregulation of the default healing process.
“In some cases, as will be discussed in further detail, prolonged inflammation and remodeling leading to fibrosis or hypertrophic scar formation may occur due to dysregulation of the default healing process [32,86,101,102].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [32]
A major event at the switch is a change in macrophage phenotype from inflammatory M1 to anti-inflammatory M2.
“One of the major events at this time is a change in the phenotype of macrophages from an inflammatory and microbicidal phenotype, grouped as M1 macrophages, secreting IL-1, TNFα, IL-6, IL-12, MMPs, and other cytokines, to an anti-inflammatory, regulatory, and reparative phenotype, classed and grouped as M2, producing arginase, TGFβ, CCL18, PGE2, and IL-10 (Fig. 4).”
From The Innate Immune System in Acute and Chronic Wounds (2016) · cites this paper as [93]
Chronic inflammation and persistent Mp accumulation are often associated with tissue destruction and fibrosis.
“However, chronic inflammation and persistent Mp accumulation are often associated with tissue destruction and fibrosis [6 -8].”
From Macrophage phenotypes during tissue repair (2013) · cites this paper as [8]
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- Authors
- Murray, P. J., & Wynn, T. A.
- Affiliations
- St. Jude Children's Research Hospital (US)
- National Institutes of Health (US)
- Corresponding author
- Murray, Peter J.
- Wynn, Thomas A.
- Venue
- Nature Reviews Immunology
- Published
- 2011-10-14
- Volume
- 11
- Issue
- 11
- Pages
- 723-737
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- PMC
- PMC3422549
- OpenAlex
- W1985859986
- Cited by
- 5,269
- References
- 178
- Citations by year
- 2026: 300 · 2025: 355 · 2024: 374 · 2023: 403 · 2022: 423 · 2021: 421 · 2020: 379 · 2019: 353 · 2018: 336 · 2017: 363 · 2016: 381 · 2015: 395 · 2014: 362 · 2013: 265 · 2012: 147
- FWCI
- 22.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (P 30CA 21765, P30CA021765)
- National Institute of Allergy and Infectious Diseases (Z01AI001019, ZIAAI001019, ZIAAI000829, Z01AI000829)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- macrophage heterogeneity, macrophage plasticity, macrophage polarization, tissue homeostasis, inflammation, macrophage recruitment, antimicrobial defense, antitumor immunity, obesity, allergy, asthma, carcinogenesis, autoimmunity, atherosclerosis, fibrosis, wound healing
- MeSH terms
- Bacterial Infections, Humans, Inflammation, Macrophage Activation, Macrophages, Neoplasms, Phagocytosis, Signal Transduction, Models, Immunological, Cell Proliferation
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