Negative Regulation of Type I IFN Expression by OASL1 Permits Chronic Viral Infection and CD8+ T-Cell Exhaustion
Figure 5
Production of sustained IFN-I and higher IRF7 protein in Oasl1 KO mice early after LCMV CL-13 infection and the cellular sources of the IFN.
WT and Oasl1 KO mice were infected with LCMV CL-13 and their sera (A), spleens (B–C), and sorted splenic cells (D) were analyzed. (A) The levels of IFN-α and IFN-β in the sera were measured by ELISA. Line graphs are shown as mean ± SD. The data are representative of at least four independent experiments (n>5 per group in each experiment). (B) mRNAs prepared from the spleens were analyzed by quantitative RT-PCR at the indicated days: mRNA expression levels (n = 3 per group) normalized to Gapdh was recalculated by dividing each expression value with the least mRNA expression value among the samples and shown as a relative mRNA level. (C) The protein levels for OASL1, IRF7, IRF3, and β-actin (loading control) were measured by immunoblot. (D) mRNA expression levels of IFN-I and OASL1 for the sorted cell populations following the sorting strategy shown in Figure S9. The mRNA expression level (n = 3 per group) of Ifna2, Ifna5/6/13, Ifnb1, or Oasl1 normalized to Gapdh was shown as a relative mRNA level. All bar graphs show mean + SD. Data of (B–D) are representative of two independent experiments. ns, not significant; *, P<0.05; **, P<0.01; ***, P<0.001.