Figure 2. Knockout of NLRP11 enhances the production of IFN‐β and antiviral responses.

• A, B
  Wild‐type (WT) and NLRP11 knockout (KO) 293T cells were transfected with an ISRE (A) or IFN‐β (B) promoter reporter plasmid and pRL‐TK plasmid for 24 h, and then transfected with poly(I:C) (5 μg/ml) (A), poly(dA:dT) (5 μg/ml), or infected with Sendai virus (SeV) (MOI = 0.1) for 20 h, followed by ISRE‐ or IFN‐β‐dependent luciferase activity (fold induction) analysis.
• C
  WT and NLRP11 KO THP‐1 cells were infected with SeV (MOI = 1) for indicated time points, and total and phosphorylated (p‐) IRF3 were analyzed by immunoblot analysis. Numbers between two blots indicate densitometry of phosphorylated proteins relative to that of total proteins, respectively.
• D
  WT and NLRP11 KO THP‐1 cells were infected with SeV (MOI = 1) for 20 h, and then, IFNB1, ISG54, and ISG56 induction were measured by real‐time PCR.
• E, F
  WT and NLRP11 KO THP‐1 cells were infected with VSV‐eGFP (MOI = 10) for 12 h or 18 h, followed by phase‐contrast (PH) and fluorescence microscopy analysis (E) and flow cytometric analysis (F). Numbers above bracketed lines indicated the percentage of VSV‐eGFP‐infected cells. Scale bar, 100 μm.

Data information: Data in (A, B, and D) are expressed as means ± SEM of three independent experiments (***P < 0.001 versus WT cells with the same treatment, Student's t‐test). Source data are available online for this figure.