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. Author manuscript; available in PMC: 2013 Nov 15.
Published in final edited form as: Clin Cancer Res. 2012 Aug 29;18(22):6110–6121. doi: 10.1158/1078-0432.CCR-12-2130

Figure 3. The presence or absence of brain tumor-derived IDO contextually regulates T cell infiltration and long-term survival in T cell -competent, but not -deficient mice.

Figure 3

Wild-type (WT) mice were intracranially-injected (ic.) 4×105 GL261 cells transduced with -scrambled shRNA (vector control, Vc; white bars) or -shRNA specific to IDO (IDO knockdown, IDOkd; black bars). Naïve (control; grey bars) mice were used as a baseline of normal T cell levels in the brain. The (A) frequency and (B) absolute numbers of total CD4+ T cells, CD8+ T cells and CD4+FoxP3+ regulatory T cells isolated from the brain of tumor-bearing mice were analyzed from naïve, or at 1, 2 and 3 weeks post-injection. All T cell populations were initially identified by the expression of CD3. Bar graphs in figures A – B are shown as mean ± SEM and are representative of two independent experiments (n = 4 – 5 mice/group). Kaplan-Meier survival curves for (C) WT, CD4-deficient (CD4−/−; lack CD4+ T cells), CD8-deficient (CD8−/−; lack CD8+ T cells) and recombinase activating gene 1-deficient (Rag1−/−; lack all functional T or B cells) mice ic. 4×105 Vc or IDOkd GL261 cells. Mouse survival was analyzed for up to 150 days (n = 7 – 16 mice/group) and reflects the pooled data resulting from 2 – 3 independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001.