FIG 7.

Loss of TSC1 alters CD8 cell effector-memory differentiation and promotes contraction. Mice received both naive WT and TSC1 KO OT1 T cells were infected with Lm-Ova in a fashion similar to that described in Fig. 3. (A) Representative fluorescence-activated cell sorter plots showing KLRG1 and IL-7Rα staining within WT OT1 and TSC1 KO OT1 populations in the peripheral blood and spleen on day 7 after infection. (B) Ratio of SLECs to MPECs within WT OT1 and TSC1 KO OT1 populations in the peripheral blood and spleen at week 1 postinfection. (C) Frequency of WT OT1 or TSC1 KO OT1 cells surviving in the peripheral blood and spleen at week 2 postinfection, as a percentage of the cells that were present at week 1. (D) T-bet and Eomes mRNA levels. Total RNA from sorted donor WT and TSC1 KO OT1 T cells 7 days after infection was subjected to reverse transcription and real-time quantitative PCR. (E) IFN-γ-producing cells within a donor OT1 T cell population. Seven days after infection, splenocytes were stimulated with SIINFEKL peptide in the presence of GolgiPlug for 5 h. The bar graph shows percentages of donor OT1 T cells that stained positive for IFN-γ. Unstim, unstimulated. All of the bar graphs represent the mean ± the standard error of the mean calculated for five mice per group. The data shown are representative of four (A to C), two (D), and three (E) independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001 (Student t test).