ArticleFrontiers in immunology2024
Inhibition SIRT1 to regulate FOXP3 or RORγt can restore the balance of Treg/Th17 axis in ulcerative colitis and enhance the anti-inflammatory effect of moxibustion.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Unravelling the role of the non-coding RNAs PVT1/miR-181a in orchestrating IL-23/RORγt and FOXP3/IL-10 axes in thrombocytopenia associated with systemic lupus erythematosus: insights into the clinical paradox of antiphospholipid syndrome.Molecular biology reports · 2026Article
- ILC2-derived IL-9 activates regulatory T cells to facilitate post-myocardial infarction repair.Cell communication and signaling : CCS · 2026Article
- RNF213 marks a regulatory T-cell subset associated with ulcerative colitis.Frontiers in immunology · 2026Article
- Gegen Qinlian Decoction, a classic traditional Chinese medicine formula: a potential therapeutic strategy for ulcerative colitis and colorectal cancer.Frontiers in pharmacology · 2026Review
- Taming autoimmune thyroiditis: cellular immunomodulation through MSCs, Tregs, and tolDCs.Frontiers in immunology · 2026Review
- Revisiting Tregs in cancer and beyond: immunological control and therapeutic potential.Frontiers in immunology · 2025Review
- Immune dysregulation in ulcerative colitis: pathogenic mechanisms and therapeutic strategies of traditional Chinese medicine.Frontiers in cell and developmental biology · 2025Review
- SIRT1: potential target in glucocorticoid-resistant diseases.Frontiers in immunology · 2025Review
- Personalized immunization to optimize vaccine immunogenicity: exploring the multidimensional effects of host intrinsic factors, external intervention strategies, and the external environment.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Ulcerative colitis (UC) is a chronic inflammatory disease. Patients with UC typically exhibit disruption of the Treg/Th17 immune axis, but its exact mechanism is still unclear. Methods: This study first analyzed RNA- seq data from public databases of humans and mice, and Results: The results show that Treg/Th17 axis disruption is an important feature of UC. Differential gene expression and immune infiltration analysis showed that upstream transcription factors, including Forkhead box P3 (FOXP3), were significantly disrupted. Conclusion: Our research shows that inhibition SIRT1 can regulate Treg and Th17 immune balance axis. This finding indicates a new important potential target for the treatment of UC.
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