MCPIP1 is a positive regulator of type I interferons antiviral activity
- Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province, 215123 (China)
- Department of Intensive Care Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, 215123 (China)
Highlights: • MCPIP1 promotes innate antiviral immunity independently of its RNase activity. • MCPIP1 enhances IFN-I mediated antiviral activity. • MCPIP1 is an IFN-induced positive feedback signal for IFN signaling activation. • MCPIP1 promotes ISRE promoter activity and ISGs expression in IFN signaling. Type-I interferons (IFN-I) are widely used for antiviral immunotherapy in clinic. Therefore, identification of the regulators of IFN-I antiviral activity is important for developing novel targets for IFN-based antiviral therapy. Monocyte chemoattractant protein 1-induced protein 1 (MCPIP1) is critical for cellular inflammatory responses. However, the roles of MCPIP1 in interferons (IFNs)-mediated antiviral immunity are unexplored. In this study, we demonstrate for the first time that MCPIP1 is an important positive regulator of IFNs antiviral activity. We found that MCPIP1 can promote innate antiviral immunity independently of both its RNase and deubiquitinase activity. Furthermore, we reveal that MCPIP1 is an IFN-induced positive feedback signal molecule which promotes IFN-I-mediated antiviral efficacy. Mechanistically, MCPIP1 does not affect the activation of JAK/STAT upstream of IFN-I signaling, but significantly promotes IFN-I signaling by enhancing ISRE promoter activity and expression of interferon-stimulated genes (ISGs). And MCPIP1-mediated activation of IFN-I signaling is independently of its RNase and deubiquitinase activity. These findings uncover a novel innate antiviral mechanism mediated by the IFN-MCPIP1 axis, and may provide potential targets for enhancing IFNs antiviral therapy.
- OSTI ID:
- 23137221
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 498, Issue 4; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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