E3 ubiquitin ligase RNF6 promotes antiviral immune responses through enhancing the expression of interferon stimulated genes in myeloid cells.

Clin Immunol

Department of Respiratory and Critical Care Medicine, Jinling Hospital, Medical School of Southeast University, Nanjing, China; Department of Respiratory and Critical Care Medicine, Jinling Hospital, Nanjing Medical University, Nanjing, China; Department of Respiratory and Critical Care Medicine, Jinling Hospital, Medical School of Nanjing University, Nanjing, China. Electronic address:

Published: September 2022

Interferon signaling is closely associated with clearance of viral infections as well as the development of systemic lupus erythematosus (SLE). Therefore, from a clinical perspective, it is important to identify the key regulators involved in interferon signaling pathways. In this study, we identified that RNF6, as an interferon inducible E3 ubiquitin ligase, promoted the interferon-dependent antiviral response. Knock-down of RNF6 greatly attenuated expression of ISGs and the transcriptional activity of ISRE. Specifically, increased RNF6 expression in myeloid cells of patients with SLE correlated with high expression of ISGs. Our results uncover RNF6 as a positive mediator in the antiviral immune responses and suggest that RNF6 may contribute to predict interferon signaling in SLE.

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Source
http://dx.doi.org/10.1016/j.clim.2022.109099DOI Listing

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