(A–C) 10⁷ splenocytes from LCMV-gp33/H-2D^b–specific TCR-Tg 318 mice were transferred i.v. into Alb-1⁺ Ifnar^–/– mice (C57BL/6 background) and littermate controls (Alb-1⁺ Ifnar^+/– or Alb-1⁺ Ifnar^+/+) on day –1. Recipients were immunized with 200 pfu LCMV on day 0. (A) On day 7, Alb-1⁺ Ifnar^–/– mice died, and livers were analyzed for CD8⁺ T cell infiltration and LCMV nucleoprotein (LCMV-NP) by immunohistology (magnification, ×100). (B) CD8⁺ T cells were analyzed by tetramer staining and in an in vitro CTL assay. (C) Serum was analyzed for bilirubin concentrations, alkaline phosphatase activity (a marker for bile cholestasis), and ALT activity (n = 3 per group). (D) Ifnar^–/– mice (Sv129 background without transfer of 318 T cells) and corresponding control mice were infected with 200 pfu LCMV-WE. After 7 days, livers were analyzed for expression of CXCL9. *P > 0.05. (E–H) 10⁷ splenocytes from LCMV-gp33/H-2D^b–specific TCR-Tg 318 mice were transferred i.v. into naive Alb-1 mice or C57BL/6 mice on day –1. Recipients were then infected with 200 PFU LCMV-WE on day 0. One group was further treated with 0.5 μg of PTX on days 0 and 3. (E) On day 6, liver sections were analyzed for CD8⁺ T cell infiltration or for viral antigen (LCMV-NP) by histology (magnification, ×100; n = 2 per group). Serum was analyzed for bilirubin concentration and ALT activity (n = 4 per group) (F), and CD8⁺ T cell effector function was assessed by an in vitro CTL assay (G). (H) Autoreactive CD8⁺ T cells and their IL-7Rα expression were analyzed in the blood (n = 4 per group).