Figure 3. The anti-viral effects of IRF-1 are neither driven by the adaptive immune responses nor by the hematopoietic cells.

A, WT and IRF-1^−/− mice were infected intranasally with 5×10⁶ pfu VSV and serum samples were collected at the indicated time points. IgM and IgG titers were quantitated by the virus neutralization assay. B/C/D, WT and IRF-1^−/− mice were lethally irradiated and reconstituted with bone marrow from IRF-1^−/− or WT mice, respectively. After 6–8 weeks, chimeric mice were infected intranasally with 5×10⁶ pfu VSV. B, Survival was monitored and plotted as Kaplan-Meier curves (n = 8–10). Data are representative of two independent experiments. Survival differences were tested for statistical significance by the log-rank test, * p<0.05. C,D Leukocytes were isolated from brains of chimeric mice (n = 6–9) 6 days post infection, stained for CD45.1 and CD8, and analyzed by flow cytometry, C, Representative flow cytometry profiles of WT CD8⁺ T cells from donor hematopoietic cells in the recipient irradiated WT and IRF-1^−/− mice. D, Total cell numbers for infiltrating donor WT CD8+ T cells in the brains of recipient WT and IRF-1^−/− mice.