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. 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 8. TRIM21 mediates an inflammatory response in primary human and mouse cells.

Figure 8

(a) Immunoblot for TRIM21 and β-actin in normal human lung fibroblasts (NHLF) treated with control (NC) or TRIM21-directed (T21) siRNA. NF-κB luciferase reporter induction in control or TRIM21-directed siRNA (si) treated NHLF after treatment with (b) LPS or (c) AdV complexed with goat polyclonal antibody (pAb) or human serum IgG (huIgG) or RSV complexed with Synagis or huIgG. Data are represented as fold increase in NF-κB induction of virus-antibody complex over PBS-treated virus. For both adenovirus antibodies, P < 0.01, n=6, unpaired t-test (*); for both RSV antibodies, the difference was not significant (N.S.). (d) NHLF NF-κB luciferase induction after treatment with the indicated inibitors. Untreated (UT), panepoxydone (PPD), 5Z-7-oxozeaenol (5Z7O), IKK inhibitor (IKK VII), Syk inhibitor (Syk I). For panels b-d error bars represent SEM of six replicates. (e) ELISA showing IL-6 concentration in supernatant of NHLFs treated with DMSO or inhibitors PPD or 5Z7O. The concentration of IL-6 produced was significantly reduced after TRIM21 knockdown P < 0.001, n=3, unpaired t-test (**). (f) DNA binding ELISA showing binding of NF-κB subunits p65 and p50 4 h post-infection in bone marrow derived macrophages (BMDM) collected from C57BL/6 WT or Trim21−/− mice aged 8-10 weeks. (g) ELISA showing cytokine concentration in supernatant from BMDM 72 h post-challenge. Error bars in panels e-g represent SEM of three replicates.