Journal
VIRAL IMMUNOLOGY
Volume 30, Issue 8, Pages 582-589Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/vim.2017.0043
Keywords
SOD2; ROS; antiviral response; RIG-I-like receptor; interferon
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Funding
- National Natural Science Foundation of China [81370464, 81671393]
- Doctoral Fund of Ministry of Education of China [20130071120031]
- Shanghai Hospital Development Center [SHDC12014221]
- Shanghai Municipal Commission of Health and Family Planning, Key Developing Disciplines [2015ZB0501]
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Superoxide dismutase 2 (SOD2) is essential in radical scavenging, which balances the intracellular level of reactive oxygen species (ROS). The dysfunction of SOD2 is associated with increasing incidence of various human diseases, including cancer, neuron diseases, and myocardial defects. However, the connections between SOD2-mediated oxidative homeostasis and innate immune response remain unclear. In this study, we report that SOD2 is a crucial regulator of antiviral signaling. Depletion of SOD2 impairs RNA virus-induced type I interferon (IFN) and proinflammatory cytokine production, resulting in enhanced viral replication. Type I IFN production is highly sensitive to cellular level of ROS. SOD2 deficiency-mediated ROS accumulation potently inhibits RIG-I-like receptor (RLR)-induced innate immune responses through the regulation of nuclear factor-kappa B (NF-B) and interferon regulatory factor-3 activation. These findings uncover a novel role for SOD2 in regulating RLR-mediated antiviral innate immune signaling.
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