Diversity, Mechanisms, and Significance of Macrophage Plasticity
Open accessAbstract
Macrophages are a diverse set of cells present in all body compartments. This diversity is imprinted by their ontogenetic origin (embryonal versus adult bone marrow–derived cells); the organ context; by their activation or deactivation by various signals in the contexts of microbial invasion, tissue damage, and metabolic derangement; and by polarization of adaptive T cell responses. Classic adaptive responses of macrophages include tolerance, priming, and a wide spectrum of activation states, including M1, M2, or M2-like. Moreover, macrophages can retain long-term imprinting of microbial encounters (trained innate immunity). Single-cell analysis of mononuclear phagocytes in health and disease has added a new dimension to our understanding of the diversity of macrophage differentiation and activation. Epigenetic landscapes, transcription factors, and microRNA networks underlie the adaptability of macrophages to different environmental cues. Macrophage plasticity, an essential component of chronic inflammation, and its involvement in diverse human diseases, most notably cancer, is discussed here as a paradigm.
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In fibrosis, macrophages have a pivotal role as regulators of pathology, where, depending on their activation state, they have been proposed to drive either fibrogenic or fibrolytic processes.
“In fibrosis, macrophages have a pivotal role as regulators of pathology, where, depending on their activation state, they have been proposed to drive either fibrogenic or fibrolytic processes (7, 10).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [10]
The “Origin” section describes macrophages as regulators of extracellular-matrix remodeling and says IL-4- or IL-13-activated macrophages can promote fibrosis. It does not describe macrophages driving fibrolytic processes, so the proposed activation-state-dependent role in both directions is only partly supported. Page numbers are unavailable in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredHepatic macrophages form a heterogeneous and highly dynamic compartment, adopting diverse activation states that extend far beyond the classical M1/M2 paradigm.
“Recent advances demonstrate that hepatic macrophages form a heterogeneous and highly dynamic compartment, adopting diverse activation states that extend far beyond the classical M1/M2 paradigm.”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [10]
The 'Macrophage plasticity: priming, polarized activation, training and tolerance' section says macrophages have diverse, adaptable activation states beyond the M1/M2 dichotomy. The 'Origin, diversity and homeostatic function' section identifies Kupffer cells as liver macrophages, but does not establish that the hepatic macrophage compartment specifically has the heterogeneity and dynamics claimed. Page numbers are not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredActivation of signal transducer and activator of transcription (STAT) is the key signaling required for macrophage polarization.
“Though several signaling involved in M2 polarization including JAK/STAT, PI3K/Akt, and AMPK pathway, activation of signal transducer and activator of transcription (STAT) is the key signaling required for macrophage polarization 72, 73.”
From Nicotinamide phosphoribosyltransferase prompts bleomycin-induced pulmonary fibrosis by driving macrophage M2 polarization in mice (2024) · cites this paper as [72]
The ‘Epigenetic marks of macrophage activation and polarization’ section (page unavailable) describes STAT6-dependent mechanisms in IL-4-induced alternative (M2) polarization. The ‘Role of post-transcriptional control’ section (page unavailable) also links suppression of JAK1/STAT6 signaling to reduced M2-type cytokines. These passages support a role for STAT signaling in M2 polarization, but do not establish that STAT activation is the key signaling required for macrophage polarization generally. (LLM, conf=0.86)
Experimental — accuracy not yet measuredM2 macrophages are induced by IL-4 and IL-13 to upregulate IL-10 and FIZZ-1 and secrete less IL-12 and nitric oxide, weakening the phagocytosis of pathogenic microorganisms.
“M2 macrophages are induced by IL-4 and IL-13 to upregulate IL-10 and FIZZ-1 and secrete less IL-12 and nitric oxide, weakening the phagocytosis of pathogenic microorganisms (Locati et al., 2020;Yunna et al., 2020;Witherel et al., 2021).”
From Nanosilver alleviates foreign body reaction and facilitates wound repair by regulating macrophage polarization (2023) · cites this paper as Locati et al., 2020
The sections on macrophage plasticity and adaptation to the tumor microenvironment (pages unavailable) identify IL-4 and IL-13 as drivers of M2 or M2-like activation. The post-transcriptional-control section reports reduced iNOS and IL-12 alongside M2 markers in a specific microRNA-related context. Our copy does not establish the claimed IL-10 and FIZZ-1 upregulation or that these changes weaken phagocytosis of pathogenic microorganisms. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMacrophage activation should not be classified as an on/off light switch system (e.g., M1/M2), but rather as a continuous spectrum of activation states.
“Thus, these recent transcriptomic, proteomic, and epigenetic studies have demonstrated that macrophage activation should not be classified as an on/off light switch system (e.g., M1/M2), but rather as a continuous spectrum of activation states (10, 30).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [10]
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- Authors
- Locati, M., Curtale, G., & Mantovani, A.
- Affiliations
- University of Milan (IT)
- Humanitas University (IT)
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2020-01-24
- Volume
- 15
- Issue
- 1
- Pages
- 123-147
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC7176483
- OpenAlex
- W2974291499
- Semantic Scholar
- cd335b98b1c4c353fc08bb29c0acebabbd2c5968
- Cited by
- 2,199
- References
- 164
- Citations by year
- 2026: 306 · 2025: 479 · 2024: 520 · 2023: 396 · 2022: 301 · 2021: 144 · 2020: 51 · 2019: 1
- FWCI
- 10.90
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- macrophage plasticity, macrophage heterogeneity, macrophage polarization, M1/M2 macrophages, trained immunity, mononuclear phagocytes, macrophage differentiation, epigenetic regulation, microRNA networks, transcription factors, chronic inflammation, cancer, tissue damage
- MeSH terms
- Cell Plasticity, Animals, Humans, Immunity, Innate, Inflammation, Macrophage Activation, Macrophages, Neoplasms, Transcription Factors, Signal Transduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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