Figure 2
Figure 2. DCs are the principle cell type presenting antigen and driving T-cell activation 1 week after LCMV infection in WT and prf−/− mice. (A) LCMV-specific CD8+ effector T cells (P14 transgenic) were cultured at the indicated ratios with either purified DCs (CD11c+) or non-DC APCs (depleted of CD11c+ and TCR+ cells) obtained from the spleens of prf−/− mice 6 days after LCMV infection. Production of IFN-γ by effector T cells was measured in culture supernatants at 24 hours. IFN-γ production was not detected when APCs were cultured with T cells of irrelevant specificity (OT1) (see Figure 3). (B) WT and prf−/− mice were irradiated and reconstituted with prf+/+/CD11cDTR or prf−/−/CD11cDTR, bone marrow, respectively. Animals were infected with LCMV and treated on days 5 and 6 with either phosphate-buffered saline (PBS) or DT. On day 7, splenic CD8+ T cells producing IFN-γ in vivo were measured (as in Figure 1). *P < .05; **P < .01.

DCs are the principle cell type presenting antigen and driving T-cell activation 1 week after LCMV infection in WT and prf−/− mice. (A) LCMV-specific CD8+ effector T cells (P14 transgenic) were cultured at the indicated ratios with either purified DCs (CD11c+) or non-DC APCs (depleted of CD11c+ and TCR+ cells) obtained from the spleens of prf−/− mice 6 days after LCMV infection. Production of IFN-γ by effector T cells was measured in culture supernatants at 24 hours. IFN-γ production was not detected when APCs were cultured with T cells of irrelevant specificity (OT1) (see Figure 3). (B) WT and prf−/− mice were irradiated and reconstituted with prf+/+/CD11cDTR or prf−/−/CD11cDTR, bone marrow, respectively. Animals were infected with LCMV and treated on days 5 and 6 with either phosphate-buffered saline (PBS) or DT. On day 7, splenic CD8+ T cells producing IFN-γ in vivo were measured (as in Figure 1). *P < .05; **P < .01.

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