STAT6 is required for IL-4 mediated attrition of VV-specific CD8⁺ T cell responses.

<p>BALB/c STAT6 ^−/− (n = 4) and BALB/c WT control mice (n = 5) were infected with 5×10⁶ PFU of VV-HA, VV-HA-IL-4 or kept unimmunized for 7 days prior to sacrifice and analysis using ICS after <i>in vitro</i> peptide stimulation. A and B, Representative dot plots showing IFN-γ and TNF-α expression on gated CD8⁺ splenocytes from infected BALB/c WT (A) or BALB/c STAT6 ^−/− (B) mice following <i>in vitro</i> stimulation of splenocytes with the indicated peptides. C, The mean (n = 4–5) number of cytokine producing K^dA52_75–83 or K^dF2_26–34 specific CD8⁺ splenocytes and the mean (n = 4–5) proportion of CD8⁺ splenocytes that produced TNF-α in addition to IFN-γ from BALB/c WT (top row of plots) or BALB/c STAT6 ^−/− (bottom row of plots) mice infected with the indicated virus. The data are representative of two independent experiments and the error bars depict the SEM. One-way ANOVA (Tukey's Multiple Comparison) was used to determine statistical significance of the data relative to VV-HA infected mice (* - p<0.05; ** - p<0.01; *** - p<0.001).