Impaired IFN-β signaling and antiviral responses in TRIM26 transgenic mice.

<p>(A–B) Expression of IFN-β mRNA and secretion of IFN-β protein measured by QRT-PCR and ELISA, respectively, in peritoneal macrophages from TRIM26-Tg and WT mice stimulated with LPS and poly(I:C) or infected with SeV and VSV for indicated times. (C) Peritoneal macrophages from TRIM26-Tg and WT mice were infected with VSV (MOI, 0.1) for 12 h. Supernatants were analyzed for VSV titers with standard plaque assays. (D) ELISA analyses of IFN-β production in sera, lung or liver from TRIM26-Tg and WT mice intravenously infected with VSV for 72 h. (n = 4 mice per group). (E) TRIM26-Tg and WT mice were infected with VSV as in D. VSV titers in lung and liver were determined by standard plaque assays (right). Expression of VSV G protein was analyzed by western blot with VSV-G antibody (left). (F) Hematoxylin and eosin staining of lung tissue sections from TRIM26-Tg and WT mice infected with VSV as in e. (G) Survival of TRIM26-Tg and WT mice (n = 10) infected with VSV (4×10⁷ pfu/mouse). Data are representative of three independent experiments (mean ± S.D. of triplicates in A-D).