[Updated Figure 7 from original manuscript]. TIR-domain-containing adapter-inducing interferon-β (TRIF) deficiency attenuates inflammation via TANK-binding kinase (TBK)1/ IκB kinase (IKK)ε and nuclear factor (NF)- κB signaling. Western blot results for wild-type (WT) and trif
−/− microglia pre-stimulated by injured retinal ganglion cells (RGCs) in a transwell system identifies the signaling changes downstream of TRIF. (A) Bar graph showing that TBK1 was upregulated gradually in the WT group; however, trif
−/− effectively suppressed TBK1 from 24 to 36 hours. (B) Trif
−/− effectively suppressed NF-κB from 12 to 36 hours. (C) Bar graph showing that trif
−/− effectively suppressed IKKε from 12 to 36 hours. *P<0.05, **P<0.01 vs. WT group at the same time point. β-Actin was used as an internal control.