Skip to main content
. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Nat Immunol. 2013 Mar 3;14(4):327–336. doi: 10.1038/ni.2548

Figure 6. TRIM21 promotes NF-κB signaling in response to viral and bacterial pathogens.

Figure 6

(a) NF-κB luciferase reporter induction in response to infection with feline calicivirus (FCV) with feline (fe) serum IgG in wild-type (WT) or Trim21-deficient (K21) MEFs. (b) Respiratory syncytial virus (RSV) with Synagis (Syn) or human (hu) serum IgG in Trim21-deficient MEFs expressing human TRIM21 (K21 T21) or empty vector (K21 EV). (c) Confocal micrographs of HeLa cells 4 h post-infection with Ab-coated GFP-expressing Salmonella enterica serovr Typhimurium (S. Typhimurium). Staining is for anti-LPS Ab and TRIM21. (d) NF-κB luciferase reporter induction in HeLa treated with control (NC) or TRIM21-directed (T21) siRNA 7 h post-challenge with Salmonella in the presence of increasing concentrations of anti-LPS Ab. (e) NF-κB luciferase reporter induction after challenge of wild-type or Trim21-deficient MEFs with Salmonella, LPS or TNF. (f) NF-κB luciferase induction in wild-type or Trim21-deficient MEFs after challenge with Ab-coated wild-type and ΔSifA Salmonella over uncoated bacteria. (g) NF-κB luciferase induction after infection of wild-type MEF or Trim21-deficeint MEFs with a dilution series of ΔSifA Salmonella incubated with PBS or anti-LPS Ab. For panels a, b, d-g, error bars represent SEM from three replicates.