ArticleCell death discovery2023
IL4I1-catalyzed tryptophan metabolites mediate the anti-inflammatory function of cytokine-primed human muscle stem cells.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Compensatory pathways in tryptophan metabolism and immune regulation following IDO inhibition.Molecular biology reports · 2026Review
- Phosphorothioate antisense oligonucleotide induced innate immune activation is attenuated by tryptophan oxidation products.Nucleic acids research · 2026Article
- Effect of PMScientific reports · 2025Article
- IL-27 Modulates Mesenchymal Stem Cell Immunoplasticity for Enhanced Lupus Nephritis Therapy via the JAK1-STAT1-IDO Axis and Tryptophan Metabolic Orchestration.Research (Washington, D.C.) · 2025Article
- Global research trends in tryptophan metabolism and cancer: a bibliometric and visualization analysis (2005-2024).Frontiers in oncology · 2025Article
- Species variations in muscle stem cell-mediated immunosuppression on T cells.Scientific reports · 2024Article
- Mesenchymal stromal cells restrain the Th17 cell response via L-amino-acid oxidase within lymph nodes.Cell death & disease · 2024Article
- Association Between Indole-3-Pyruvic Acid and Change in Fat-Free Mass Relative to Weight Loss in Patients Undergoing Sleeve Gastrectomy.Metabolites · 2024Article
- IL4I1 in M2-like macrophage promotes glioma progression and is a promising target for immunotherapy.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Muscle stem cells (MuSCs) have been demonstrated to exert impressive therapeutic efficacy in disease settings through orchestrating inflammatory microenvironments. Nevertheless, the mechanisms underlying the immunoregulatory property of MuSCs remain largely uncharacterized. Here, we showed that interleukin-4-induced-1 (IL4I1), an essential enzyme that catalyzes indole metabolism in humans, was highly expressed in human MuSCs exposed to IFN-γ and TNF-α. Functionally, the MuSCs were found to inhibit the infiltration of neutrophils into sites of inflammation in a IL4I1-dependent manner and thus ameliorate acute lung injury in mice. Mechanistically, the indole metabolites, including indole-3-pyruvic acid (I3P) and indole-3-aldehyde (I3A), produced by IL4I1, acted as ligands to activate aryl hydrocarbon receptor (AHR), leading to augmented expression of TNF-stimulated gene 6 (TSG-6) in inflammatory cytokine-primed MuSCs. Furthermore, I3P administration alone suppressed neutrophil infiltration into damaged lungs. I3P could also reduce the level of reactive oxygen species in neutrophils. Therefore, our study has uncovered a novel mechanism by which MuSCs acquire their immunoregulatory property and may help to develop or optimize MuSC-based therapies for inflammatory diseases.
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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.