期刊
CELLULAR & MOLECULAR IMMUNOLOGY
卷 9, 期 6, 页码 497-502出版社
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/cmi.2012.35
关键词
innate immunity; interferon-alpha; macrophages; microRNA; miR-466l
类别
资金
- National Natural Science Foundation of China [81070880]
- China Postdoctoral Science Foundation [42201]
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-alpha) 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-alpha 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-alpha expression to inhibit host antiviral innate immune response. Cellular & Molecular Immunology (2012) 9, 497-502; doi:10.1038/cmi.2012.35; published online 8 October 2012
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