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Published on: July 23, 2012
MicroRNA-15b Suppresses Th17 Differentiation and Is Associated with Pathogenesis of Multiple Sclerosis by Targeting
Ruiqiong Liu1,2, Xiaofeng Ma1, Li Chen3
1Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Abstract:
IL-17-producing Th17 cells have gradually become considered as key factors in the pathogenesis of many autoimmune diseases, including multiple sclerosis (MS). Although the involvement of certain microRNAs in the development of MS has been reported, their role in Th17-driven autoimmunity is still poorly understood. In this study, we identified microRNA (miR)-15b as an important factor in Th17-associated effects and determined that the expression of miR-15b is significantly downregulated in MS patients and in mice with experimental autoimmune encephalomyelitis. Overexpression of miR-15b alleviated experimental autoimmune encephalomyelitis, whereas knockdown of miR-15b aggravated it. We demonstrated that miR-15b suppressed Th17 differentiation both in vivo and in vitro. We also found that O-linked N-acetylglucosamine transferase is a potential target of miR-15b, enabling it to affect the transcriptional regulation of retinoic acid-related orphan receptor γT through O-linked N-acetylglucosamine glycosylation of NF-κB. These results contribute to the importance of miR-15b in Th17 differentiation and the pathogenesis of MS.
Insights
MicroRNA-15b plays a crucial role in regulating T helper 17 cell differentiation and is downregulated in multiple sclerosis (MS). Restoring miR-15b levels can alleviate MS pathogenesis by suppressing Th17 cell activity.
Area of Science:
- Immunology
- Molecular Biology
- Neuroscience
Background:
- T helper 17 (Th17) cells are implicated in autoimmune diseases like multiple sclerosis (MS).
- The specific role of microRNAs in Th17-driven autoimmunity, particularly in MS, remains incompletely understood.
Purpose of the Study:
- To investigate the role of microRNA (miR)-15b in Th17 cell differentiation and its potential involvement in the pathogenesis of multiple sclerosis.
- To identify the molecular mechanisms by which miR-15b influences Th17-associated autoimmunity.
Main Methods:
- Expression analysis of miR-15b in MS patients and experimental autoimmune encephalomyelitis (EAE) mouse models.
- In vivo and in vitro studies involving overexpression and knockdown of miR-15b to assess its effect on EAE and Th17 differentiation.
- Identification of potential miR-15b targets and analysis of downstream signaling pathways.
Main Results:
- miR-15b expression was significantly downregulated in MS patients and EAE mice.
- Overexpression of miR-15b ameliorated EAE, while its knockdown exacerbated the condition.
- miR-15b was found to suppress Th17 cell differentiation both in vivo and in vitro.
- O-linked N-acetylglucosamine transferase was identified as a potential target of miR-15b, affecting NF-κB glycosylation and retinoic acid-related orphan receptor γT (RORγT) regulation.
Conclusions:
- miR-15b is a critical regulator of Th17 differentiation and plays a significant role in the pathogenesis of multiple sclerosis.
- Targeting miR-15b may offer a novel therapeutic strategy for managing MS and other Th17-driven autoimmune diseases.
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