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MicroRNA-466l inhibits antiviral innate immune response by targeting interferon-alpha.

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.
AuthorsYingke Li, Xiaohua Fan, Xingying He, Haijing Sun, Zui Zou, Hongbin Yuan, Haitao Xu, Chengcai Wang, Xueyin Shi
JournalCellular & molecular immunology (Cell Mol Immunol) Vol. 9 Issue 6 Pg. 497-502 (Nov 2012) ISSN: 2042-0226 [Electronic] China
PMID23042536 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • 3' Untranslated Regions
  • Interferon-alpha
  • MicroRNAs
  • Mirn466 microRNA, mouse
  • RNA, Messenger
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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