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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-?) 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-? 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-? expression to inhibit host antiviral innate immune response.

SUBMITTER: Li Y 

PROVIDER: S-EPMC4002216 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

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

Li Yingke Y   Fan Xiaohua X   He Xingying X   Sun Haijing H   Zou Zui Z   Yuan Hongbin H   Xu Haitao H   Wang Chengcai C   Shi Xueyin X  

Cellular & molecular immunology 20121008 6


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 fou  ...[more]

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