Skip to main content
. 2011 Nov 21;121(12):4889–4902. doi: 10.1172/JCI59259

Figure 6. Functional characterization of the S186L AD TRIF mutation.

Figure 6

(A) 293HEK-TLR3 cells were transfected with empty vector, WT, or S186L TRIF plasmids along with IFN-β–Luc/NF-κB–Luc and RL-TK vectors to assess IFN-β and NF-κB promoter induction upon overexpression of TRIF. Values (mean ± SEM) were calculated from at least 3 independent experiments. (B) SV40 fibroblasts from control (C+) and P1’s fibroblasts retrovirally transduced with either empty vector, WT TRIF, or S186L TRIF were stimulated with 25 μg/ml poly(I:C) for 24 hours, and the production of cytokines was assessed by ELISA. Values (mean ± SEM) were calculated from at least 3 independent experiments. (C) SV40 fibroblasts from control (C+) and P2’s fibroblasts retrovirally transduced with empty vector, WT TRIF, or S186L TRIF were stimulated with 25 μg/ml poly(I:C) for 24 hours, and the production of cytokines was assessed by ELISA. Values (mean ± SEM) were calculated from at least 3 independent experiments. (D) Replication of HSV-1 GFP was assessed after 24 hours of infection in control SV40 fibroblasts (C+); SV40 fibroblasts from P1 retrovirally transduced with empty vector, WT, or S186L TRIF; and (E) SV40 fibroblasts from P2 retrovirally transduced with empty vector, WT, or S186L. Cells were pretreated with media (left) or recombinant IFN-α (right). Values (mean ± SEM) were calculated from at least 3 independent experiments.