ArticleJCI insight2021
YY1 regulation by miR-124-3p promotes Th17 cell pathogenicity through interaction with T-bet in rheumatoid arthritis.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- T-bet: biological functions, molecular mechanisms, and therapeutic applications: a systematic review.Frontiers in immunology · 2026Pooled it
- Clonal sharing and plasticity of follicular CD4 + T cells across lymph nodes and tumors in non-small cell lung cancer.Nature communications · 2026Article
- MFAP5iScience · 2026Article
- Systemic regulation of rheumatoid arthritis by mesenchymal stem cells: from immune homeostasis to microbiota modulation.Frontiers in immunology · 2026Review
- The Role of Synovitis and Latent Transcription Factors in the Pathogenesis of Rheumatoid Arthritis.Current rheumatology reviews · 2026Review
- Single-cell transcriptomic profiling reveals aberrant CD4⁺ naive T cell differentiation driving immune activation in Behçet's uveitis.Journal of translational medicine · 2025Article
- miRNAs and T cell-mediated Immune Response in Disease.The Yale journal of biology and medicine · 2025Review
- The Role of Long Non-Coding RNA in Rheumatoid Arthritis.International journal of molecular sciences · 2025Review
- Immunomodulatory roles of quercetin in diabetic nephropathy: targeting inflammation, oxidative stress, and ferroptosis.Frontiers in pharmacology · 2025Review
- The novel role of Yin Yang 1 in acute rejection of liver allografts through activation of dendritic cells.Frontiers in immunology · 2025Article
- Quercetin through miR-147-5p/Clip3 axis reducing Th17 cell differentiation to alleviate periodontitis.Regenerative therapy · 2024Article
- Oxymatrine Ameliorates Lupus Nephritis by Targeting the YY1-Mediated IL-6/STAT3 Axis.International journal of molecular sciences · 2024Article
- AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1.Journal of biomedical research · 2024Article
- SETBP1 activation upon MDM4-enhanced ubiquitination of NR3C1 triggers dissemination of colorectal cancer cells.Clinical & experimental metastasis · 2024Article
- YY1 Lactylation Aggravates Autoimmune Uveitis by Enhancing Microglial Functions via Inflammatory Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A novel diagnostic model based on lncRNA PTPRE expression, neutrophil count and red blood cell distribution width for diagnosis of seronegative rheumatoid arthritis.Clinical and experimental medicine · 2024Article
- Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin.Scientific reports · 2024Article
- Luobitong Potentiates MTX's Anti-Rheumatoid Arthritis Activity via Targeting Multiple Inflammatory Pathways.Journal of inflammation research · 2024Article
- Hypoxia-inducible factors and essential hypertension: narrative review of experimental and clinical data.Pharmacological reports : PR · 2023Review
- Leveraging Exosomes as the Next-Generation Bio-Shuttles: The Next Biggest Approach against Th17 Cell Catastrophe.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Th17 cells are involved in rheumatoid arthritis (RA) pathogenesis. Our previous studies have revealed that transcription factor Yin Yang 1 (YY1) plays an important role in the pathogenic mechanisms of RA. However, whether YY1 has any role in Th17 cell pathogenicity and what molecular regulatory mechanism is involved remain poorly understood. Here, we found the proportion of pathogenic Th17 (pTh17) cells was significantly higher in RA than in control individuals and showed a potential relationship with YY1 expression. In addition, we also observed YY1 expression was increased in pTh17, and the pTh17 differentiation was hampered by YY1 knockdown. Consistently, knockdown of YY1 decreased the proportion of pTh17 cells and attenuated joint inflammation in collagen-induced arthritis mice. Mechanistically, YY1 could regulate the pathogenicity of Th17 cells through binding to the promoter region of transcription factor T-bet and interacting with T-bet protein. This function of YY1 for promoting pTh17 differentiation was specific to Th17 cells and not to Th1 cells. Moreover, we found miR-124-3p negatively correlated with YY1 in RA patients, and it could bind to 3'-UTR regions of YY1 to inhibit the posttranscriptional translation of YY1. Altogether, these findings indicate YY1 regulation by miR-124-3p could specifically promote Th17 cell pathogenicity in part through interaction with T-bet, and these findings present promising therapeutic targets in RA.
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