Figure 6
Figure 6. Increased T-cell activation in Ctx− mice after LCMV infection is due to heightened physiologic presentation of viral antigen. (A) Polyclonal, WT, or prf−/− (GFP+) T cells were transferred into either WT or prf−/− recipients 1 day before LCMV infection. The percentage of transferred CD8+ T cells that were producing IFN-γ+ in vivo was quantitated 6 days after infection. (B) Seven days after LCMV infection, spleens were disaggregated in collagenase and stained as indicated. Sample dot plots are shown, with the percentages of gated populations indicated (±SEM; n = 6-9 per group/stain). (C) Seven days after LCMV infection, T-cell–depleted spleen cells were plated with either LCMV-specific effector T cells (P14) or T cells of irrelevant specificity (OT1, ovalbumin) and specific IFN-γ production over background (spleen cells alone, which was < 5% of that measured in the presence of P14 T cells) was measured after 18 hours. *P < .01.

Increased T-cell activation in Ctx mice after LCMV infection is due to heightened physiologic presentation of viral antigen. (A) Polyclonal, WT, or prf−/− (GFP+) T cells were transferred into either WT or prf−/− recipients 1 day before LCMV infection. The percentage of transferred CD8+ T cells that were producing IFN-γ+ in vivo was quantitated 6 days after infection. (B) Seven days after LCMV infection, spleens were disaggregated in collagenase and stained as indicated. Sample dot plots are shown, with the percentages of gated populations indicated (±SEM; n = 6-9 per group/stain). (C) Seven days after LCMV infection, T-cell–depleted spleen cells were plated with either LCMV-specific effector T cells (P14) or T cells of irrelevant specificity (OT1, ovalbumin) and specific IFN-γ production over background (spleen cells alone, which was < 5% of that measured in the presence of P14 T cells) was measured after 18 hours. *P < .01.

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