TBK1 and IKK epsilon(IKKi) are described as essential regulators of pathogen-triggered IFN gene activation through the direct phosphorylation of IFN regulatory factors.
Embryonic fibroblast cells from TBK1-deficient mice show decreased IRF3 activation and IFN induction by poly IC, while IKKi-deficient cells show normal IRF3 activation. However, the activation of IRF3 is totally abolished in TBK1 and IKKi double-deficient cells, indicating that the functions of TBK1 and IKKi are redundant in mouse embryo fibroblast cells.[Hemmi et al 2004].
TBK1/IKKi interact with SIKE (Suppressor of IKK epsilon), which was shown to act as an inhibitor of TBK1/IKKi-mediated type I IFN production, but not NF-kB activation signaling[Huang J et al 2005].