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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
miR26a modulates Th17/T reg balance in the EAE model of multiple sclerosis by targeting IL6
Rongwei Zhang1, Ayong Tian, Jun Wang
1Department of Gerontology and Geriatrics, The First Affiliated Hospital of China Medical University, No. 155, Nanjing North Street, Heping District, Shenyang, 110001, Liaoning, China, rongweizhang@126.com.
Abstract:
A number of different microRNAs (miRNAs) have been implicated in various autoimmune diseases, including multiple sclerosis (MS). T helper (Th)17 and regulatory T cells (Tregs) have likewise been implicated as key players in MS, and a functional imbalance of these cell types is increasingly recognized as a key etiological factor in the disease. Although specific panels of transcription factors and cytokines are known to regulate the Th17/Treg balance, the role of noncoding RNAs remains poorly understood. The inflammatory cytokine, interleukin (IL)6, appears to play a critical role in both the development of the Th17 response and the inhibition of Treg functions. In this research, an IL6-associated miRNA, miR26a, was identified, and its normally downregulated expression was shown to be highly correlated with disease severity in patients suffering from MS as well as in C57BL/6 mice with experimental autoimmune encephalomyelitis (EAE; a well-established animal model of human MS). Using the EAE model system, in vivo silencing of miR26a was found to result in increased expression of Th17-related cytokines and increased severity of EAE, while overexpression of miR26a was found to result in reduced expression of Th17-related cytokines and a milder form of EAE. By contrast, Treg cell-specific transcription factor, Foxp3, was found to be positively correlated with miR26a expression. Finally, miR26a was found to downregulate Th17 and to upregulate Treg cell function through its targeting of IL6. Taken together, our data indicate an important role for miR26a in maintaining the Th17 and Treg cell balance in MS that involves repression of IL6 expression.
Insights
MicroRNA 26a (miR26a) plays a crucial role in balancing T helper 17 (Th17) and regulatory T cells (Tregs) in multiple sclerosis (MS). Its downregulation correlates with disease severity, suggesting miR26a as a potential therapeutic target.
Area of Science:
- Immunology
- Molecular Biology
- Neuroscience
Background:
- MicroRNAs (miRNAs) are implicated in autoimmune diseases like multiple sclerosis (MS).
- T helper 17 (Th17) and regulatory T cells (Tregs) are key players in MS pathogenesis, with their imbalance contributing to disease.
- The role of noncoding RNAs, such as miRNAs, in regulating the Th17/Treg balance in MS is not well understood.
Purpose of the Study:
- To investigate the role of miR26a in the context of Th17/Treg cell balance in multiple sclerosis (MS).
- To explore the relationship between miR26a expression, disease severity in MS, and its potential to target interleukin-6 (IL6).
Main Methods:
- Utilized the experimental autoimmune encephalomyelitis (EAE) mouse model, a standard model for MS.
- Assessed miR26a expression levels in relation to disease severity in both MS patients and EAE mice.
- Manipulated miR26a levels (silencing and overexpression) in the EAE model to observe effects on Th17/Treg cells and disease progression.
- Investigated the correlation between miR26a and the Treg-specific transcription factor Foxp3.
- Examined the direct targeting of IL6 by miR26a.
Main Results:
- miR26a expression was downregulated and correlated with MS and EAE severity.
- Silencing miR26a increased Th17 cytokines and EAE severity; overexpression reduced Th17 cytokines and ameliorated EAE.
- miR26a expression positively correlated with Foxp3, a marker for Treg cells.
- miR26a was shown to downregulate Th17 cell function and upregulate Treg cell function by targeting IL6.
Conclusions:
- miR26a plays a significant role in maintaining the Th17/Treg cell balance in MS.
- miR26a exerts its function by repressing IL6 expression, thereby modulating immune responses relevant to MS.
- miR26a represents a potential therapeutic target for managing MS by restoring immune homeostasis.
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