Figure 7. Prdm1 deficiency rescues the development of Tcf7^−/− CD8⁺ T cells with the stem-like phenotype but not their recall potential.

(A) Representative flow plots showing expression of SLAMF6 and TIM3 in WT, Tcf7^−/−, Prdm1^−/−, and Tcf7^−/−/Prdm1^−/− gp33-specific CD8⁺ T cells from spleens of LCMV-c13 infected mice on 21 dpi (n = 9 for WT, n = 3 for Prdm1^−/−, n = 4 for Tcf7^−/−, and n = 3 for Tcf7^−/−/Prdm1^−/− mice).

(B) Pooled data from two experiments shown as mean ± SD and p values analyzed by one-way ANOVA and Dunnett’s multiple comparisons test (n = 9 for WT, n = 3 for Prdm1^−/−, n = 4 for Tcf7^−/−, and n = 3 for Tcf7^−/−Prdm1^−/− mice).

(C) Volcano plot of RNA-seq results from WT and Tcf7^−/−/Prdm1^−/− Tpex (n = 4) with cutoffs by adjusted p < 0.0001 and fold-change > 2.

(D) Heatmaps of selected genes of WT and Tcf7^−/−/Prdm1^−/− Tpex isolated 21 dpi with LCMV-c13 (n = 4).

(E) GO analysis of differentially expressed genes.

(F) Plasma LCMV gp transcript abundance in LCMV-c13 infected WT, Tcf7^−/−, Prdm1^−/−, and Tcf7^−/−/Prdm1^−/− mice (n = 16 for WT, n = 5 for Prdm1^−/−, n = 6 for Tcf7^−/−, and n = 7 for Tcf7^−/−/Prdm1^−/− mice). Data from three experiments, shown as medians and analyzed by one-way ANOVA.

(G) Schematic representation of transfer experiment to test recall responses of Tpex, pertaining to (H).

(H) Fold-expansion of donor-derived (CD45.2) gp33-specific CD8⁺ T cells of each genotype 7 days after rechallenge, pooled from three experiments (n = 13 for WT, n = 7 for Prdm1^−/−, n = 4 for Tcf7^−/−, and n = 9 for Tcf7^−/−/Prdm1^−/−), shown as mean ± SD and analyzed by one-way ANOVA and Dunnett’s multiple comparisons test.

See also Figure S7.