MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis
Abstract
Interleukin 17 (IL-17)-producing T helper cells (T(H)-17 cells) are increasingly recognized as key participants in various autoimmune diseases, including multiple sclerosis. Although sets of transcription factors and cytokines are known to regulate T(H)-17 differentiation, the role of noncoding RNA is poorly understood. Here we identify a T(H)-17 cell-associated microRNA, miR-326, whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). In vivo silencing of miR-326 resulted in fewer T(H)-17 cells and mild EAE, and its overexpression led to more T(H)-17 cells and severe EAE. We also found that miR-326 promoted T(H)-17 differentiation by targeting Ets-1, a negative regulator of T(H)-17 differentiation. Our data show a critical role for microRNA in T(H)-17 differentiation and the pathogenesis of multiple sclerosis.
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miR-326 has been implicated as a pro-inflammatory miRNA in circulating CD4+ T cells.
“miR-326 has been implicated as a pro-inflammatory miRNA in circulating CD4+ T cells21”
From CNS microRNA profiles: a database for cell type enriched microRNA expression across the mouse central nervous system (2020) · cites this paper as [21]
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- Authors
- Du, C., Liu, C., Kang, J., Zhao, G., Ye, Z., Huang, S., Li, Z., Wu, Z., & Pei, G.
- Venue
- Nature Immunology
- Published
- 2009-10-18
- Volume
- 10
- Issue
- 12
- Pages
- 1252-1259
- ISSN
- 1529-2908
- 1529-2916
- Cited by
- 711
- References
- 10
- Language
- en
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