ArticleProceedings of the National Academy of Sciences of the United States of America2022
TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
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- A who's who of cell types in skeletal muscle.Communications biology · 2026Review
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Macrophage programming in systemic sclerosis: Niches, networks, and translational horizons.Seminars in immunopathology · 2026Review
- Sarcopenia, an independent predictor for all-cause mortality in rheumatoid arthritis: Insights from the NHANES database.Medicine · 2026Article
- Macrophages and the Survival of Cardiomyocytes After Myocardial Infarction.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Article
- Skeletal muscle as a dynamic immunological niche for vaccination.Frontiers in immunology · 2026Review
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Cancer-driven cytokine immunomodulation ameliorates cardiac function and suppresses fibrosis.Journal of molecular and cellular cardiology plus · 2025Article
- Establishment of disseminated neonatal echovirus 11 infection model in hFcRn transgenic mice.Virology journal · 2025Article
- Radiation-induced impairment of skeletal muscle regeneration.Radiology and oncology · 2025Review
- M2-ApoBDs as a therapeutic strategy for systemic lupus erythematosus: targeted macrophage reprogramming and treg differentiation.Journal of nanobiotechnology · 2025Article
- Stem cell activity shapes the pleiotropic effects of IFN-γ and TGF-β in autoimmune diseases, infections, and cancer, and drives autoimmune flares and remissions.Frontiers in immunology · 2025Review
- Evaluating the immunogenicity of a mouse partial hindlimb for composite allotransplantation.Frontiers in immunology · 2025Article
- Skeletal Muscle and the Immune System.Advances in experimental medicine and biology · 2025Review
- A pairwise cytokine code explains the organism-wide response to sepsis.Nature immunology · 2024Article
- The complex heterogeneity of immune cell signatures across wasting tissues with C26 and 5-fluorouracil-induced cachexia.American journal of physiology. Cell physiology · 2024Article
- DPPIVNature communications · 2023Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
Abstract
IFNγ is traditionally known as a proinflammatory cytokine with diverse roles in antimicrobial and antitumor immunity. Yet, findings regarding its sources and functions during the regeneration process following a sterile injury are conflicting. Here, we show that natural killer (NK) cells are the main source of IFNγ in regenerating muscle. Beyond this cell population, IFNγ production is limited to a small population of T cells. We further show that NK cells do not play a major role in muscle regeneration following an acute injury or in dystrophic mice. Surprisingly, the absence of IFNγ per se also has no effect on muscle regeneration following an acute injury. However, the role of IFNγ is partially unmasked when TNFα is also neutralized, suggesting a compensatory mechanism. Using transgenic mice, we showed that conditional inhibition of IFNGR1 signaling in muscle stem cells or fibro-adipogenic progenitors does not play a major role in muscle regeneration. In contrast to common belief, we found that IFNγ is not present in the early inflammatory phase of the regeneration process but rather peaks when macrophages are acquiring an anti-inflammatory phenotype. Further transcriptomic analysis suggests that IFNγ cooperates with TNFα to regulate the transition of macrophages from pro- to anti-inflammatory states. The absence of the cooperative effect of these cytokines on macrophages, however, does not result in significant regeneration impairment likely due to the presence of other compensatory mechanisms. Our findings support the arising view of IFNγ as a pleiotropic inflammatory regulator rather than an inducer of the inflammatory response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.