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. 2015 Nov 19;43(5):974–986. doi: 10.1016/j.immuni.2015.10.013

Figure 7.

Figure 7

Blockade of Type I Interferon Signaling Ameliorates Oxidative Stress-Induced Liver Pathology upon Viral Infection

(A) RAW264.7 macrophages and primary hepatocytes from WT mice were infected with LCMV (MOI 5) and co-treated with 20 μg/ml blocking antibody α-IFNAR1 or isotype control. 24 hr later cells were stained with CellROX. Scale bar represents 20 μm. Representative images are shown. Quantification was performed by CellProfiler and numbers represent mean ± SEM. The group of unstimulated hepatocytes is the same as used for Figure 5E. One out of ≥ two similar experiments is shown.

(B) WT mice respectively Sod1−/− mice, which received either isotype control or α-IFNAR1 blocking antibody, were infected with LCMV. Serum kinetics of ALT was measured (n = 4 mice per group). One out of ≥ two similar experiments is shown.

(C) Atf3 mRNA in the liver was measured 72 hr after LCMV infection from mice treated as described in (B).

(D) WT mice received either isotype control or α-IFNAR1 blocking antibody and were infected with LCMV. Serum kinetics of ALT was measured (n = 9 or 10 mice pooled from two experiments).

(E) Atf3 mRNA in the liver was measured 45 hr after LCMV infection from mice treated as described in (D).

Statistical significance was calculated by one-way (A and C) or by two-way ANOVA (B and D) with Bonferroni correction and (E) with unpaired t test. Symbols and bars represent the mean ± SEM.