ArticleJournal of advanced research2025
Sp3 ameliorated experimental autoimmune encephalomyelitis by triggering Socs3 in Th17 cells.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Plasma Proteomics Identifies Proteins and Pathways Associated with Cataract: A Prospective Cohort Study.Ophthalmology science · 2026Article
- Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors.bioRxiv : the preprint server for biology · 2025Article
- Bulk RNAseq Analysis of Cardiac Myosin-Specific CD4Biomedicines · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
introductionAlthough it is believed that chronic inflammatory and degenerative diseases of the central nervous system are mediated by autoimmune Th17 cells, the underlying mechanisms remain largely unexplored. Recent studies and our research have revealed that Sp3 was blocked in multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE). However, it remained unclear why it is silent and how it regulates Th17 cell differentiation in MS.
objectivesThis study aimed to explore the impact of Sp3 on Th17 cell-mediated EAE and the underlying mechanism.
methodsThe effect of Sp3 on the clinical symptoms of EAE was evaluated by scoring, histochemistry, and fast blue (FB) techniques, scRNA-seq data analysis, flow cytometry, ELISA, PCR, WB, immunofluorescence and reporter gene techniques were used to explore the molecular mechanism of Sp3 regulating Th17 cell differentiation.
resultsInjection of overexpression Sp3 lentivirus could significantly ameliorate the EAE progress and clinical symptoms and prevent the polarization of Th1 and Th17 cells both in vivo and in vitro. We confirmed the occurrence of EAE in Sp3
conclusionThus, our study suggests a novel mechanism involving miR-223/Sp3/Socs3/TGF-β signaling as a potential therapeutic strategy for targeting Th17 cells in immunotherapy.
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