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Significance LncRNAs have been identified as regulating antiviral innate responses via different targets through various ways. Whether there is an abundant and highly conserved lncRNA in the nucleus which may regulate antiviral innate signaling through a new mechanism remains to be investigated. Here, we identify that viral infection-reduced expression ofMalat1 feedback promotes IRF3-initiated type I IFN production in the innate response against viral infection.Malat1 binds to TDP43 and prevents its cleavage mediated by activated caspase-3. The cleaved TDP35 inhibits IRF3 degradation through promoting the degradation of pre-mRNA of Rbck1, an E3 ubiquitin ligase targeting IRF3. AberrantMALAT1 reduction and IRF3 activation are found in SLE patients, providing one mechanistic explanation for why SLE patients always have type I interferonopathies.

LncRNA Malat1 inhibition of TDP43 cleavage suppresses IRF3-initiated antiviral innate immunity