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IL-10 Triggers Changes in Macrophage Phenotype That Promote Muscle Growth and Regeneration
Open accessAbstract
We examined the function of IL-10 in regulating changes in macrophage phenotype during muscle growth and regeneration following injury. Our findings showed that the Th1 cytokine response in inflamed muscle is characterized by high levels of expression of CD68, CCL-2, TNF-α, and IL-6 at 1 d postinjury. During transition to the Th2 cytokine response, expression of those transcripts declined, whereas CD163, IL-10, IL-10R1, and arginase-1 increased. Ablation of IL-10 amplified the Th1 response at 1 d postinjury, causing increases in IL-6 and CCL2, while preventing a subsequent increase in CD163 and arginase-1. Reductions in muscle fiber damage that normally occurred between 1 and 4 d postinjury did not occur in IL-10 mutants. In addition, muscle regeneration and growth were greatly slowed by loss of IL-10. Furthermore, myogenin expression increased in IL-10 mutant muscle at 1 d postinjury, suggesting that the mutation amplified the transition from the proliferative to the early differentiation stages of myogenesis. In vitro assays showed that stimulation of muscle cells with IL-10 had no effect on cell proliferation or expression of MyoD or myogenin. However, coculturing muscle cells with macrophages activated with IL-10 to the M2 phenotype increased myoblast proliferation without affecting MyoD or myogenin expression, showing that M2 macrophages promote the early, proliferative stage of myogenesis. Collectively, these data show that IL-10 plays a central role in regulating the switch of muscle macrophages from a M1 to M2 phenotype in injured muscle in vivo, and this transition is necessary for normal growth and regeneration of muscle.
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“In mouse skeletal muscle injury by chemical toxin or unloading/reloading, IL-4 mRNA, although detectable, does not rise above uninjured levels over the course of healing [73,74].”
From Macrophage phenotypes during tissue repair (2013) · cites this paper as [73]
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“The phenotypic switch of the macrophages is mediated by IL10, which also promotes myoblast differentiation and fiber formation [21].”
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Chen, J., & Li, Q. (2024) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2024.1368171 · Cited by 4
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Khan, M. A., Bhusal, S., Lau, C. L., & Krupnick, A. S. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1567657 · Cited by 6
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“CD68 is expressed on macrophages and labels early-invading macrophages that accumulate in injured skeletal muscle (Rabinowitz and Gordon 1991; Holness et al. 1993; Deng et al. 2012).”
BackgroundSkeletal Muscle Damage and Inflammation
Washington, T. A., & Schrems, E. R. (2025) · Advances in experimental medicine and biology · doi:10.1007/978-3-031-88361-3_9 · Cited by 5
Jian, Z., Yang, D., Tang, C., Zheng, L., Zhao, W., Zhou, Z., Wang, F., & Peng, X. (2025) · Stem Cell Reviews and Reports · doi:10.1007/s12015-025-10969-7 · Cited by 4
“Furthermore, MSCs produce Interleukin-10 (IL-10) to induce the transition of M1 macro - phages to M2 and recruit Treg cells to fight inflammation to support subsequent muscle generation [64, 66, 67].”
From quiescence to repair: C/EBPβ as a regulator of muscle stem cell function in health and disease
AlSudais, H., & Wiper‐Bergeron, N. (2021) · FEBS Journal · doi:10.1111/febs.16307 · Cited by 3
Haptoglobin as a novel predictor of visceral involvement and relapse in adult IgAV patients
Bajželj, M., Visočnik, N., Mrak‐Poljšak, K., Hladnik, M., Lakota, K., & Hočevar, A. (2025) · Clinical Rheumatology · doi:10.1007/s10067-025-07363-6 · Cited by 3
“While IL-6 is the major stimulus for haptoglobin synthesis [34], CD163 expression is chiefly dependent on IL-10 [35].”
Bone Marrow Myeloid–Lymphatic Progenitors Expand Tumor Lymphatic Vasculature Through Cell Fusion
Athaiya, S., Volk-Draper, L. D., Cox, E., Robinson, K., Zinkevich, N. S., & Ran, S. (2025) · Cancers · doi:10.3390/cancers17111804 · Cited by 3
“However, IL-10 knockout mice are deficient in generation of multinucleated osteoclasts [110] and muscle fibers [111] which leads, respectively, to bone and muscle loss.”
Therapeutic strategies for critical limb ischemia: a focus on endogenous cell behavior modulation
Wang, H., Wang, X., Liu, C., & Liu, C. (2025) · Journal of Materials Chemistry B · doi:10.1039/d5tb01357g · Cited by 3
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Inflammatory response of the peripheral neuroendocrine system following downhill running
Minari, A. L. A., Avila, F., Oyama, L. M., & dos Santos, R. V. T. (2021) · Cytokine · doi:10.1016/j.cyto.2021.155746 · Cited by 3
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“Finally, macrophage polarization from M1 to M2 phenotypes supports regenerative myogenesis—delivery of IL-4 or IL-10 to injured muscle skews macrophages toward an M2 profile, creating a pro-regenerative microenvironment that synergizes with reprogramming cues [80].”
Molecular Mechanisms and Nutritional Modulation in Sarcopenia: A Narrative Review
Chin, H. S., Liu, L., Liao, P.-J., Wee, A. L. R. M., Kwek, X.-Y., Teh, B. T., & Koh, F. H.-X. (2026) · Nutrients · doi:10.3390/nu18071161 · Cited by 3
“Muscle regeneration relies on a “regenerative switch” where regulatory T cells (Tregs) and IL-10 drive macrophages from the pro-inflammatory (M1) to a pro-regenerative (M2) phenotype, essential for IGF-1 secretion during myogenesis [36–40].”
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Efficacy of red low-level laser for postoperative pain management: A review of literature
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“In vivo data have shown that IL-10 plays a central role in regulating the switch of muscle macrophages from an M1 to M2 phenotype in injured muscle in vivo, and this transition is necessary for normal growth and regeneration of muscle (Deng et al 2012).”
BackgroundInflammatory response induced by resistance exercise
Vasconcelos, E. D. S. (2018) · MOJ Immunology · doi:10.15406/moji.2018.06.00204 · Cited by 4
Huschtscha, Z., Young, P., Parr, A., Porter, J. A., & Costa, R. J. S. (2022) · PLoS ONE · doi:10.1371/journal.pone.0274210 · Cited by 2
“Studies in-vivo have indicated that IL-10 plays an integral role activating macrophages from the M1 (pro-inflammatory) to the M2 (anti-inflammatory) phenotype [32], thus supporting the observations of the current study.”
BackgroundResultMuscular Dystrophy - Research Updates and Therapeutic Strategies
Gaina, G. F. (2020) · IntechOpen eBooks · doi:10.5772/intechopen.87261 · Cited by 1
Lokwani, R., Ngo, T. B., DeStefano, S., Adusei, K. M., Bhuiyan, M., Josyula, A., Faust, M. T., Lin, A., Karkanitsa, M. L., Fathi, P., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.08.19.504399 · Cited by 2
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Increased Cytokine Levels in Seronegative Myositis: Potential Th17 Immune Response Implications
Aguilar-Vázquez, A., Chavarría-Ávila, E., Gutiérrez-Hernández, J. M., Toríz, G., Salazar-Páramo, M., Medrano-Ramírez, G., Vargas-Cañas, E. S., Pizano-Martínez, Ó., Gomez-Rios, C.-A., Juarez-Gomez, C., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252011061 · Cited by 1
HDAC11 deficiency regulates age-related muscle decline and sarcopenia
Odria, R., Cardús, A., Gomis-Coloma, C., Balanyà-Segura, M., Mercado-Amarilla, A., Maestre-Mora, P., Sabuco, A. P., Domingo, J. C., Nogales‐Gadea, G., Gomez-Sanchez, J. A., et al. (2025) · GeroScience · doi:10.1007/s11357-025-01611-y · Cited by 1
“…in homeostasis and in injury, the muscle stem cell pool is protected HDAC11 epigenetic target identified [48–50], and it is a key factor in regulating myogenic differentiation in vivo [55], where it has been reported that its supplementation increases muscle strength, mass, and myofiber size [56].”
Mitochondria in the immune system: Therapeutic potential from mitochondria transfer
Le, T. H. N., & Nguyen, V. T. T. (2025) · International Reviews of Immunology · doi:10.1080/08830185.2025.2577986 · Cited by 1
“M1 macrophages produce nitric oxide (NO), inflammatory mediators, and cytokines in response to pro-inflammatory factors to combat microbial infection [87], while M2 macrophages become anti-inflammatory in response to IL-4, with the ability to support tissue recovery [88].”
Odria, R., Mercado-Amarilla, A., Soler‐Botija, C., Borràs, D., Ohana, J., Maestre-Mora, P., Bigot, A., Suárez‐Calvet, X., Gallardo, E., Nogales‐Gadea, G., et al. (2025) · Life Sciences · doi:10.1016/j.lfs.2025.124150 · Cited by 1
Hua, L., Wang, Y., Yuan, X., Wang, R., Li, X., Fan, Y., Hou, Z., Yang, L., Liu, T., & Sun, Q. (2026) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2026.121444 · Cited by 1
Tuning Secretomes for Regenerative Medicine
Buschmann, J. (2026) · Biology · doi:10.3390/biology15120941 · Cited by 2
Macrophage plasticity and metabolic control in muscle repair and disease
Tiufekchiev-Grieco, S., Novak, J. S., & Jaiswal, J. K. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1872583 · Cited by 1
“For instance, FAPs increase their expression of Il10 following muscle injury which is a cytokine involved in initiating an ARM-like polarization of macrophages (16, 80, 81).”
Meeting Report: New Directions in Biology and Disease of Skeletal Muscle 2014
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Immune System Regulation of Muscle Injury and Disease
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Muscular Dystrophy and Rehabilitation Interventions with Regenerative Treatment
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Role of muscle stem cells in sarcopenia
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Metadata
- Authors
- Deng, B., Wehling-Henricks, M., Villalta, S. A., Wang, Y., & Tidball, J. G.
- Affiliations
- University of California, Los Angeles (US)
- Department of Integrative Biology and Physiology, University of California , Los Angeles, Los Angeles, CA 90095
- Corresponding author
- Deng, Bo
- Wang, Ying
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-10-01
- Volume
- 189
- Issue
- 7
- Pages
- 3669-3680
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3448810
- OpenAlex
- W2153554828
- Cited by
- 472
- References
- 68
- Citations by year
- 2026: 24 · 2025: 25 · 2024: 26 · 2023: 33 · 2022: 43 · 2021: 40 · 2020: 41 · 2019: 44 · 2018: 32 · 2017: 43 · 2016: 43 · 2015: 28 · 2014: 27 · 2013: 22 · 2012: 1
- FWCI
- 9.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Muscular Dystrophy Association (157881)
- National Institutes of Health (R01 AR/AG054451)
- National Institute on Aging (R01 AR/AG054451)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR047855, R01AR054451, R01AR047721)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Keywords
- IL-10, muscle regeneration, muscle growth, macrophage polarization, M2 macrophages, M1 macrophages, Th1/Th2 shift, muscle damage, myogenesis, myoblast proliferation, arginase-1, CD163, myogenin, MyoD, MCP-1, TNF-α, interleukin-6
- MeSH terms
- Animals, Female, Macrophages, Mice, Inbred C57BL, Regeneration, Up-Regulation, Immunophenotyping, Cytokines, Interleukin-10, Mice, Knockout, Th1 Cells, Th2 Cells, Muscle, Skeletal, Cell Enlargement, Cell Proliferation, Mice, Mice, 129 Strain
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