Excessive IFNγ production in LCMV-infected pfp^–/– mice is driven by persistent antigen presentation to CD8⁺ T cells. (A) Ten days after LCMV infection, antigen-specific CD8⁺ T cells from wild-type and pfp^–/– mice were quantitated by MHC-peptide tetramer (Db-GP33) staining and intracellular IFNγ staining (after stimulation with GP33 peptide). (B) Relative staining intensity for IFNγ was quantitated in wild-type and pfp^–/– CD8 T cells after in vitro stimulation with peptide (GP33). MFI indicates mean fluorescence intensity. (C) Spontaneous IFNγ production by CD8⁺ T cells obtained 6 days after LCMV infection was assessed in wild-type and pfp^–/– mice by intracellular staining in the absence of stimulating peptide. (D) Viral titers were measured in wild-type and pfp^–/– spleens 6 days after LCMV infection. (E) Serum IFNγ levels were assayed at day 12 in pfp^–/– mice that had been given either control or LCMV-neutralizing antibody 4 to 6 days after infection. (F) Survival was monitored in these same mice. (G) Wild-type mice were given GP33 peptide (250 mcg every 12 hours, intraperitoneally) starting 4 days after LCMV infection. Serum IFNγ levels were assayed at days 6 and 12 and plotted with the time course from Figure 5A for comparison. (H) Relative macrophage infiltrates (% CD68⁺) in various tissues and blood cellularity were compared between wild-type mice that did or did not receive GP33 peptide after LCMV infection (assayed at day 12). WBC indicates white blood cells; Plts, platelets; and Hgb, hemoglobin. Data (± standard error) are representative of at least 2 experiments with at least 3 mice in each group.