Macrophage plasticity and polarization in tissue repair and remodelling
Abstract
Mononuclear phagocyte plasticity includes the expression of functions related to the resolution of inflammation, tissue repair and remodelling, particularly when these cells are set in an M2 or an M2 ‐like activation mode. Macrophages are credited with an essential role in remodelling during ontogenesis. In extraembryonic life, under homeostatic conditions, the macrophage trophic and remodelling functions are recapitulated in tissues such as bone, mammary gland, decidua and placenta. In pathology, macrophages are key components of tissue repair and remodelling that occur during wound healing, allergy, parasite infection and cancer. Interaction with cells bearing stem or progenitor cell properties is likely an important component of the role of macrophages in repair and remodelling. These properties of cells of the monocyte–macrophage lineage may represent a tool and a target for therapeutic exploitation.
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Physical properties (substrate stiffness, topography, pore size, size of wear debris), chemical properties (surface chemistry, ligand presentation, release of growth factors), and temporal properties (degradation rates) all influence cell behavior.
“Physical properties such as substrate stiffness, topography, pore size and size of wear debris; chemical properties such as surface chemistry, ligand presentation and release of growth factors; and temporal properties, such as degradation rates, all influence the behavior of cells [8,9].”
From Biomaterial based modulation of macrophage polarization: a review and suggested design principles (2015) · cites this paper as [9]
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 [94]
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- Authors
- Mantovani, A., Biswas, S. K., Galdiero, M. R., Sica, A., & Locati, M.
- Affiliations
- University of Milan (IT)
- Agency for Science, Technology and Research (SG)
- University of Naples Federico II (IT)
- Università degli Studi del Piemonte Orientale “Amedeo Avogadro” (IT)
- Corresponding author
- Mantovani, Alberto
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2012-11-29
- Volume
- 229
- Issue
- 2
- Pages
- 176-185
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W1797422316
- Cited by
- 2,384
- References
- 144
- Citations by year
- 2026: 126 · 2025: 137 · 2024: 189 · 2023: 192 · 2022: 244 · 2021: 223 · 2020: 203 · 2019: 196 · 2018: 172 · 2017: 184 · 2016: 165 · 2015: 154 · 2014: 124 · 2013: 72 · 2012: 2
- FWCI
- 10.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Pathology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- macrophage plasticity, macrophage polarization, M2 macrophages, tissue repair, tissue remodeling, inflammation resolution, wound healing, monocyte/macrophage lineage, ontogeny, placenta, decidua, mammary gland, bone remodeling, allergy, parasitic infection, cancer, therapeutic target
- MeSH terms
- Animals, Cell Differentiation, Homeostasis, Humans, Inflammation, Macrophage Activation, Macrophages, Neoplasms, Phenotype, Stem Cells, Wound Healing, Inflammation Mediators
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