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. 2012 Apr 19;8(4):e1002633. doi: 10.1371/journal.ppat.1002633

Figure 4. High incidence of AFN in PV+LCMV double immune mice following PV re-challenge.

Figure 4

(A) Naïve, PV-immune, and (PV+LCMV WT) double immune mice were re-challenged with PV, sacrificed 3 days PI, and the severity of AFN in the visceral fat pads was assessed. (*) indicates p<.05 in frequency of AFN using the Kruskai-Wallis test (one-way ANOVA non-parametric). (B), (C), and (D) represent experiments performed using the LCMV clone 13 system and its naturally derived V207A mutant. (B) Domination of NP205-specific CD8 T cells in PV+Clone 13 LCMV WT double immune mice. PBL were collected from double-immune mice, before the final challenge with PV, and stimulated with peptides ex vivo in a standard ICS assay. These are representative frequencies of the IFNγ positive CD8α+ T cells from 4 independent experiments using 5 mice per group. (C) Incidence of AFN after PV challenge. Naïve, (PV+Clone 13 LCMV WT), and (PV+Clone 13 LCMV NP-V207A) double immune mice re-challenged with PV were sacrificed 4 days PI, and the severity of AFN in the visceral fat pads was assessed. Compilation of data from 4 independent experiments. (*) and (***) indicate p<.05 and p<.0001, respectively. (D) Domination of cross-reactive NP205-specific CD8 T cells isolated from the visceral fat pad of (PV+Clone 13 LCMV WT) double immune mice following PV re-challenge. Standard ICS and FACs analyses were performed. Numbers are representative frequencies of IFNγ+, CD8α+ T cells from two similar experiments.