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Tyrosine kinase 2 (TYK2) is a member of the Janus kinase (JAK) family and is involved in cytokine signalling.  In vitro  analyses suggest that TYK2 also has kinase-independent, i.e., non-canonical, functions. We have generated gene-targeted mice harbouring a mutation in the ATP-binding pocket of the kinase domain. The  Tyk2  kinase-inactive ( Tyk2 K923E  ) mice are viable and show no gross abnormalities. We show that kinase-active TYK2 is required for full-fledged type I interferon- (IFN) induced activation of the transcription factors STAT1-4 and for the  in vivo  antiviral defence against viruses primarily controlled through type I IFN actions. In addition, TYK2 kinase activity was found to be required for the protein’s stability. An inhibitory function was only observed upon over-expression of TYK2 K923E   in vitro. Tyk2 K923E   mice represent the first model for studying the kinase-independent function of a JAK  in vivo  and for assessing the consequences of side effects of JAK inhibitors.

TYK2 Kinase Activity Is Required for Functional Type I Interferon Responses In Vivo