Fig. 2
From: Virus-specific memory T cells populate tumors and can be repurposed for tumor immunotherapy
Antiviral T-cell reactivation promotes intratumoral immune activation. a Volcano plot of differentially expressed genes determined by RNAseq from whole B16 tumors 9 h after peptide exposure. Orange and blue circles are significantly (q-value < 0.05) upregulated (>1.5 log2FC) or downregulated genes (<−1.5 log2FC), respectively, compared to irrelevant peptide treated tumors (n = 3 mice; data from one experiment). b Proportion of CD86 +/CCR7 + CD103+ DCs in tumor at 12 h (n = 6 mice for irrelevant, n = 5 mice for viral), and tumor draining (dLN) or non-draining (ndLN) LN at 48 h (n = 7) following intratumoral irrelevant (black circles) or viral SIINFEKL peptide (red circles). c Quantification of CD103 + DCs in LN at 48 h. n = 6 mice (irrelevant), n = 7 mice (viral). d Proportion of B16 tumor cells expressing MHC I at 24 h. n = 5 mice (irrelevant), n = 6 mice (viral). e Quantification of NK cells and CD44hi CD8+ T cells (excluding OT-I) in Braf/Pten tumors (48 h). n = 6 mice (CD8), and n = 7 mice (NK). f Enumeration of granzyme B + NK and non-viral peptide-specific CD8+ T cells in Braf/Pten tumors. Example of granzyme B staining in NK cells (inset) at 48 h; n = 7 mice. All data, unless indicated, are pooled from at least two independent experiments. Significance was determined by unpaired two-tailed Mann–Whitney test (e, CD8); and unpaired two-tailed t-test (b, tumor) d, and (e, NK), and a one-way unpaired ANOVA with Tukey post hoc test (b, LN) and (c). Lines represent means and error bars are SEM. *p < 0.05, **p < 0.01, ***p < 0.001
