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SUMO2 and SUMO3 redundantly prevent a noncanonical type I interferon response [Immunology and Inflammation]

Type I interferons (IFNs) are cytokines that are essential for host defense against virus infection, but when they are inappropriately produced, they can cause severe autoimmune disease in humans. We have found that the sumoylation pathway of protein modification is essential for preventing an ectopic IFN response. Specifically, we have identified SUMO2 and SUMO3 as the two SUMO proteins that redundantly prevent IFN production. Remarkably, the potent IFN response caused by loss of SUMO2/3 is independent of all known inducers of the antiviral response, revealing a distinct mechanism of IFN production that has implications for our understanding of antiviral immunity.

Authors:   John T. Crowl; Daniel B. Stetson
Journal:   Proceedings of the National Academy of Sciences current issue
Volume:   115
edition:   26
Year:   2018
Pages:   6798
DOI:   10.1073/pnas.1802114115
Publication date:   26-Jun-2018
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