Inducible microRNA-155 Feedback Promotes Type I IFN Signaling in Antiviral Innate Immunity by Targeting Suppressor of Cytokine Signaling 1
Open accessAbstract
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-κB–dependent pathway. And the inducible miR-155 feedback promotes type I IFN signaling, thus suppressing viral replication. Furthermore, suppressor of cytokine signaling 1 (SOCS1), a canonical negative regulator of type I IFN signaling, is targeted by miR-155 in macrophages, and SOCS1 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 SOCS1.
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In a viral infection model, miR-155 is induced via a TLR/MyD88-independent, RIG-I/JNK/NF-κB-dependent pathway, downregulating SOCS1 and enhancing type I IFN signaling, potentially exacerbating inflammation.
“It was shown that in a model of viral infection, miR-155 expression is induced in a TLR/MyD88-independent but retinoic acid-inducible gene I/JNK/NF-κB-dependent pathway, which leads to downregulation of suppressor of cytokine signaling 1 (SOCS1), and thus enhancement of type I IFN signaling, which may exacerbate inflammation [210].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [210]
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- Authors
- Wang, P., Hou, J., Lin, L., Wang, C., Liu, X., Li, D., Ma, F., Wang, Z., & Cao, X.
- Affiliations
- Second Military Medical University (CN)
- Zhejiang University (CN)
- Shanghai Jiao Tong University (CN)
- Corresponding author
- Wang, Pin
- Hou, Jin
- Wang, Chunmei
- Liu, Xingguang
- Cao, Xuetao
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-11
- Volume
- 185
- Issue
- 10
- Pages
- 6226-6233
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2143216993
- Cited by
- 431
- References
- 2
- Citations by year
- 2026: 7 · 2025: 14 · 2024: 13 · 2023: 17 · 2022: 25 · 2021: 31 · 2020: 33 · 2019: 37 · 2018: 29 · 2017: 35 · 2016: 38 · 2015: 33 · 2014: 46 · 2013: 31 · 2012: 33
- FWCI
- 9.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- miR-155, SOCS1, type I interferon signaling, antiviral innate immunity, macrophages, vesicular stomatitis virus, RNA virus infection, viral replication inhibition, microRNA target regulation
- MeSH terms
- Suppressor of Cytokine Signaling 1 Protein, Animals, Cell Line, Dendritic Cells, Enzyme-Linked Immunosorbent Assay, Feedback, Gene Expression Regulation, Immunity, Innate, Interferon Type I, Macrophages, Mice, Inbred C57BL, RNA Virus Infections, Virus Replication, Blotting, Western, Signal Transduction, Vesiculovirus, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, RNA Interference, MicroRNAs, Suppressor of Cytokine Signaling Proteins, Mice
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