ArticleResearch (Washington, D.C.)2025
IL-27 Modulates Mesenchymal Stem Cell Immunoplasticity for Enhanced Lupus Nephritis Therapy via the JAK1-STAT1-IDO Axis and Tryptophan Metabolic Orchestration.
Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The role of mesenchymal stem cells in IgA nephropathy: current evidence and future directions.Stem cell research & therapy · 2026Review
- Harnessing MSCs plasticity: mechanisms and determinants of bidirectional immune regulation in stem-cell-based immunotherapy.Stem cell research & therapy · 2026Review
- Rearming mesenchymal stem cells with engineering strategies to combat cancer.Frontiers in immunology · 2026Review
- The Gut Microbiota: Emerging Evidence in Autoimmune and Inflammatory Diseases.Research (Washington, D.C.) · 2026Review
- Stem Cell and Cell-Free Strategies for Osteoarthritis: Toward Durable Regenerative Therapies.Stem cells international · 2026Review
- Taming autoimmune thyroiditis: cellular immunomodulation through MSCs, Tregs, and tolDCs.Frontiers in immunology · 2026Review
- Ultrasound-guided intrarenal arterial injection promotes homing of MSCs and recovery of kidney in Adriamycin-induced nephropathy in rats.Cell transplantationArticle
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Authors and funding
11 authors.
Funding
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Abstract
Lupus nephritis is recognized as a common and severe complication of systemic lupus erythematosus, without an optimal therapeutic strategy currently available. While mesenchymal stem cells (MSCs) hold therapeutic promise, their efficacy varies substantially, likely due to their plasticity and capacity to adopt pro-inflammatory (MSC1) or anti-inflammatory (MSC2) functional states in response to different microenvironments. Here, we report for the first time that IL-27, via JAK1-STAT1 signaling, up-regulates indoleamine 2,3-dioxygenase (IDO) in MSCs, driving MSC differentiation toward an IDO-positive MSC2 phenotype with low immunogenicity. These IDO-positive MSC2 cells produce kynurenine and kynurenic acid, the metabolites of tryptophan, which bind to the intracellular aryl hydrocarbon receptor. This interaction stimulates an increase in the anti-inflammatory factor TSG-6 and induces the differentiation of regulatory T cells. Notably, IL-27-conditioned MSC2 demonstrated superior therapeutic efficacy compared to conventional MSCs in a murine lupus nephritis model. In conclusion, this study revealed that IL-27 is a critical modulator of MSC immune plasticity and presented a novel therapeutic strategy utilizing IL-27-enhanced MSC2 for autoimmune 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.