Abstract |
Effective recognition of viral infections and subsequent triggering of antiviral innate immune responses are essential for the host antiviral defense, which is tightly regulated by multiple regulators, including microRNAs ( miRNAs). A previous study showed that miR-466l upregulates IL-10 expression in macrophages by antagonizing RNA-binding protein tristetraprolin-mediated IL-10 mRNA degradation. However, the ability of miR-466l to regulate antiviral immune responses remains unknown. Here, we found that interferon-alpha (IFN-α) expression was repressed in Sendai virus (SeV)- and vesicular stomatitis virus (VSV)-infected macrophages and in dendritic cells transfected with miR-466l expression. Moreover, multiple IFN-α species can be directly targeted by miR-466l through their 3' untranslated region ( 3'UTR). This study has demonstrated that miR-466l could directly target IFN-α expression to inhibit host antiviral innate immune response.
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Authors | Yingke Li, Xiaohua Fan, Xingying He, Haijing Sun, Zui Zou, Hongbin Yuan, Haitao Xu, Chengcai Wang, Xueyin Shi |
Journal | Cellular & molecular immunology
(Cell Mol Immunol)
Vol. 9
Issue 6
Pg. 497-502
(Nov 2012)
ISSN: 2042-0226 [Electronic] China |
PMID | 23042536
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- 3' Untranslated Regions
- Interferon-alpha
- MicroRNAs
- Mirn466 microRNA, mouse
- RNA, Messenger
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Topics |
- 3' Untranslated Regions
(genetics)
- Animals
- Base Sequence
- Dendritic Cells
(immunology, virology)
- Gene Expression Regulation
- HEK293 Cells
- Humans
- Immunity, Innate
(immunology)
- Interferon-alpha
(biosynthesis, genetics, metabolism)
- Macrophages
(immunology, virology)
- Mice
- Mice, Inbred C57BL
- MicroRNAs
- RNA, Messenger
(genetics, metabolism)
- Sendai virus
(immunology)
- Transcription, Genetic
- Vesiculovirus
(immunology)
- Virus Replication
(immunology)
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