摘要
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-4661 upregulates IL-IO expression in macrophages by antagonizing RNA-binding protein tristetraprolin-mediated IL-10 mRNA degradation. However, the ability of miR-4661 to regulate antiviral immune responses remains unknown. Here, we found that interferon-alpha （IFN-a） expression was repressed in Sendai virus （SeV）- and vesicular stomatitis virus （VSV）-infected macrophages and in dendritic cells transfected with miR-4661 expression. Moreover, multiple IFN-α species can be directly targeted by miR-4661 through their 3＇ untranslated region （3＇UTR）. This study has demonstrated that miR-4661 could directly target IFN-a expression to inhibit host antiviral innate immune response.
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-4661 upregulates IL-IO expression in macrophages by antagonizing RNA-binding protein tristetraprolin-mediated IL-10 mRNA degradation. However, the ability of miR-4661 to regulate antiviral immune responses remains unknown. Here, we found that interferon-alpha （IFN-a） expression was repressed in Sendai virus （SeV）- and vesicular stomatitis virus （VSV）-infected macrophages and in dendritic cells transfected with miR-4661 expression. Moreover, multiple IFN-α species can be directly targeted by miR-4661 through their 3＇ untranslated region （3＇UTR）. This study has demonstrated that miR-4661 could directly target IFN-a expression to inhibit host antiviral innate immune response.
