Journal
JOURNAL OF IMMUNOLOGY
Volume 185, Issue 10, Pages 6226-6233Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000491
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Funding
- National 115 Key Project for Hepatitis B Virus Research [2008ZX10002-008]
- National Natural Science Foundation of China [30721091]
- National Key Basic Research Program of China [2007CB512403]
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Effective recognition of viral infection and subsequent triggering of antiviral innate immune responses are essential for the host antiviral defense, which is tightly regulated by multiple regulators, including microRNAs. Our previous study showed that a panel of microRNAs, including miR-155, was markedly upregulated in macrophages upon vesicular stomatitis virus infection; however, the biological function of miR-155 during viral infection remains unknown. In this paper, we show that RNA virus infection induces miR-155 expression in macrophages via TLR/MyD88-independent but retinoic acid-inducible gene I/JNK/NF-kappa B-dependent pathway. And the inducible miR-155 feedback promotes type I IFN signaling, thus suppressing viral replication. Furthermore, suppressor of cytokine signaling 1 (SOCSI), a canonical negative regulator of type I IFN signaling, is targeted by miR-155 in macrophages, and SOCSI knockdown mediates the enhancing effect of miR-155 on type I IFN-mediated antiviral response. Therefore, we demonstrate that inducible miR-155 feedback positively regulates host antiviral innate immune response by promoting type I IFN signaling via targeting SOCSI. The Journal of Immunology, 2010, 185: 6226-6233.
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