The role of macrophages in the resolution of inflammation
Open accessAbstract
Macrophages are tissue-resident or infiltrated immune cells critical for innate immunity, normal tissue development, homeostasis, and repair of damaged tissue. Macrophage function is a sum of their ontogeny, the local environment in which they reside, and the type of injuries or pathogen to which they are exposed. In this Review, we discuss the role of macrophages in the restoration of tissue function after injury, highlighting important questions about how they respond to and modify the local microenvironment to restore homeostasis.
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Mo-AMs, but not TR-AMs, are responsible for the pro-fibrotic activity of lung macrophages.
“Mo-AMs, but not TR-AMs, are responsible for the pro-fibrotic activity of this group of cells1,3,10,13”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [3]
The pathogenic role of Mo-AMs in lung fibrosis is largely attributed to their production of pro-fibrotic mediators such as TGF-β, PDGF-α, osteopontin, and MMPs.
“The pathogenic role of Mo-AMs in lung fibrosis has been largely attributed to their activity in producing a number of pro-fibrotic mediators, such as TGF-β, PDGF-α, osteopontin (OPN), and MMPs1,3,11,13,15,18,28.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [3]
Depletion of Mo-AMs confers protection from lung fibrosis in multiple mouse models.
“depletion of Mo-AMs via several strategies conferred protection from lung fibrosis in multiple mouse models1,3,10,11,13,20”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [3]
Only Mo-AMs, not the entire type of cells, are responsible for the detrimental role of lung macrophages in pulmonary fibrosis.
“Recent studies have made inroads into this challenge by demonstrating that it is only a subgroup, the Mo-AMs, and not the entire type of cells, that are responsible for the detrimental role of lung macrophages in pulmonary fibrosis1,3,10,13.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [3]
It remains largely unclear what regulates the pro-fibrotic potency of lung macrophages.
“it remains largely unclear what regulates their pro-fibrotic potency in the lung2,3,19–27”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [3]
Macrophages play a crucial role in the pathogenesis of lung fibrosis.
“Although it has long been recognized that macrophages play a crucial role in the pathogenesis of lung fibrosis”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [3]
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“The pathogenic role of Mo-AMs in lung fi brosis has been largely attributed to their activity in producing a number of pro-fi brotic mediators, such as TGF-β , PDGF-α , osteopontin (OPN), and MMPs 1,3,11,13,15,18,28 .”
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- Authors
- Watanabe, S., Alexander, M., Misharin, A. V., & Budinger, G. R. S.
- Affiliations
- Kanazawa University (JP)
- Northwestern University (US)
- Corresponding author
- Budinger, G.R. Scott
- Venue
- Journal of Clinical Investigation
- Published
- 2019-05-20
- Volume
- 129
- Issue
- 7
- Pages
- 2619-2628
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC6597225
- OpenAlex
- W2945953423
- Cited by
- 925
- References
- 29
- Citations by year
- 2026: 110 · 2025: 160 · 2024: 197 · 2023: 133 · 2022: 136 · 2021: 120 · 2020: 58 · 2019: 10 · 2018: 1
- FWCI
- 6.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense (PR141319)
- U.S. Department of Veterans Affairs (I01CX001777, I01 BX000201)
- Northwestern University
- National Institutes of Health (1r56hl135124-01, AG‐049665, HL-071643, AI135964)
- Feinberg School of Medicine
- National Institute on Aging (P01AG049665)
- National Heart, Lung, and Blood Institute (P01HL071643, R56 HL135124, T32HL076139)
- National Institute of Allergy and Infectious Diseases (AI135964, U19AI135964)
- National Institute of Environmental Health Sciences (R01ES013995)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- macrophages, inflammation resolution, tissue repair, tissue homeostasis, macrophage ontogeny, local microenvironment, innate immunity, tissue damage, tissue regeneration
- MeSH terms
- Animals, Homeostasis, Humans, Immunity, Innate, Inflammation, Macrophages, Regeneration
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