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Updated: Jun 13, 2026
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Altered microRNA expression profile with miR-146a upregulation in CD4+ T cells from patients with rheumatoid
Jingyi Li1, Ying Wan, Qiuye Guo
1Institute of Immunology, PLA, Third Military Medical University, 30# Gaotanyan Street, District Shipingba, Chongqing 400038, PR China.
Introduction:
Increasing evidence indicates that microRNAs (miRNAs) play a critical role in the pathogenesis of inflammatory diseases. The aim of the study was to investigate the expression pattern and function of miRNAs in CD4+ T cells from patients with rheumatoid arthritis (RA).
Methods:
The expression profile of miRNAs in CD4+ T cells from synovial fluid (SF) and peripheral blood of 33 RA patients was determined by microarray assay and validated by qRT-PCR analysis. The correlation between altered expression of miRNAs and cytokine levels was determined by linear regression analysis. The role of miR-146a overexpression in regulating T cell apoptosis was evaluated by flow cytometry. A genome-wide gene expression analysis was further performed to identify miR-146a-regulated genes in T cells.
Results:
miRNA expression profile analysis revealed that miR-146a expression was significantly upregulated while miR-363 and miR-498 were downregulated in CD4+ T cells of RA patients. The level of miR-146a expression was positively correlated with levels of tumor necrosis factor-alpha (TNF-alpha), and in vitro studies showed TNF-alpha upregulated miR-146a expression in T cells. Moreover, miR-146a overexpression was found to suppress Jurkat T cell apoptosis. Finally, transcriptome analysis of miR-146a overexpression in T cells identified Fas associated factor 1 (FAF1) as a miR-146a-regulated gene, which was critically involved in modulating T cell apoptosis.
Conclusions:
We have detected increased miR-146a in CD4+ T cells of RA patients and its close correlation with TNF-alpha levels. Our findings that miR-146a overexpression suppresses T cell apoptosis indicate a role of miR-146a in RA pathogenesis and provide potential novel therapeutic targets.
Insights
MicroRNA-146a is elevated in rheumatoid arthritis CD4+ T cells and correlates with TNF-alpha. Upregulated miR-146a suppresses T cell apoptosis, suggesting a role in RA pathogenesis and potential therapeutic targeting.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are increasingly recognized for their role in inflammatory disease pathogenesis.
- This study investigates miRNA expression and function in CD4+ T cells from rheumatoid arthritis (RA) patients.
Purpose of the Study:
- To determine the expression pattern of miRNAs in CD4+ T cells from RA patients.
- To elucidate the functional role of specific miRNAs, particularly miR-146a, in T cell apoptosis and RA pathogenesis.
Main Methods:
- Microarray and qRT-PCR were used to profile miRNA expression in CD4+ T cells from RA patients.
- Linear regression analyzed correlations between miRNA levels and cytokines (e.g., TNF-alpha).
- Flow cytometry and transcriptome analysis assessed the impact of miR-146a on T cell apoptosis and identified target genes.
Main Results:
- miR-146a was significantly upregulated, while miR-363 and miR-498 were downregulated in RA CD4+ T cells.
- miR-146a expression positively correlated with tumor necrosis factor-alpha (TNF-alpha) levels.
- Overexpression of miR-146a suppressed T cell apoptosis, with Fas associated factor 1 (FAF1) identified as a key regulated gene.
Conclusions:
- Increased miR-146a in RA CD4+ T cells is closely linked to TNF-alpha levels.
- miR-146a's ability to suppress T cell apoptosis highlights its pathogenic role in RA.
- These findings suggest miR-146a as a potential therapeutic target for rheumatoid arthritis.
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