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Stimulation of Cytoplasmic DNA Sensing Pathways In Vitro and In Vivo

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[Nucleic acids recognition by innate immunity].

Shizuo Akira¹, Tatsuya Saitoh, Taro Kawai

¹Laboratory of Host Defense, WPI Immunology Frontier Research Center (IFReC), Osaka University Department of Host Defense, Research Institute for Microbial Diseases. sakira@biken.osaka-u.ac.jp

|November 30, 2012

Summary

Tripartite-motif 56 (TRIM56) regulates DNA-mediated interferon induction by ubiquitinating STING. Viperin protein promotes type I interferon production by dendritic cells through Toll-like receptor 7 and 9 signaling.

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Area of Science:

Immunology
Molecular Biology
Virology

Background:

The innate immune system uses nucleic acid sensing to trigger host defense mechanisms, including type I interferon (IFN) production.
Pathogen-derived DNA and RNA are detected by specific sensors, initiating antiviral responses.
Type I IFNs are crucial cytokines for controlling viral infections.

Purpose of the Study:

To identify regulators of double-stranded DNA-mediated type I interferon induction.
To elucidate the role of interferon-inducible tripartite-motif (TRIM) 56 in innate immunity.
To investigate the antiviral function of Viperin in Toll-like receptor (TLR) signaling pathways.

Main Methods:

Investigated TRIM56's interaction with STING and its ubiquitination status.
Analyzed TRIM56-mediated STING dimerization and TBK1 recruitment.
Examined Viperin's expression, localization, and interaction with signaling mediators in plasmacytoid dendritic cells (pDCs).

Main Results:

TRIM56 was identified as an interferon-inducible E3 ubiquitin ligase that targets STING for K63-linked ubiquitination, promoting STING dimerization and subsequent IFN-beta induction.
Viperin expression is induced by TLR7 and TLR9 stimulation in pDCs and localizes to lipid bodies.
Viperin facilitates K63-linked ubiquitination of IRAK1 at lipid bodies, leading to IRF7 nuclear translocation and type I IFN production.

Conclusions:

TRIM56 is a key regulator of the STING-mediated pathway for double-stranded DNA sensing, crucial for innate immune responses.
Viperin enhances TLR7 and TLR9-mediated type I IFN production in pDCs by modulating the IRAK1-TRAF6 signaling axis at lipid bodies.
These findings reveal novel mechanisms by which TRIM56 and Viperin contribute to antiviral immunity.