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. Author manuscript; available in PMC: 2023 Dec 13.
Published in final edited form as: Immunity. 2022 Nov 11;55(12):2369–2385.e10. doi: 10.1016/j.immuni.2022.10.020

Figure 2. Tumor control required CD8+ T cell-intrinsic IRF2 expression.

Figure 2.

Tumor growth kinetics in WT or Irf2−/− mice that received isotype control or anti-CD8 depleting antibody either (A) one day before (early CD8+ T cell depletion) or (B) 21 days after (late CD8+ T cell depletion) MC38 initiation. For late depletion, only Irf2−/− mice were used since WT mice had already reached endpoint by day 21. Shaded region indicates duration of antibody treatment.

(C) MC38 tumor growth in WT control (i.e., Irf2+/+, purple), CD8-IRF2cWT (i.e., Irf2+/+ CD8Cre+ mice, black), CD8-IRF2cKO (IRF2-deficient only in CD8+ T cells; blue), or Irf2−/− (red) mice.

(D) Tumor size after WT mice received 2×105 naïve WT (black) or Irf2−/− (red) P14 T cells one day prior to receiving MC38-GP tumor.

(E) Tumor growth in WT or Irf2−/− mice with orthotopic PyMT breast tumor cells that were treated with isotype or anti-PDL1 blocking antibody beginning on day 15 after tumor implantation. Number in graph indicates the fold change in tumor size between the isotype vs. anti-PDL1 treatment for WT or Irf2−/− mice. Shaded region indicates duration of antibody treatment.

(F) MC38-GP tumoresize after WT mice received 2×105 pre-activated WT (black) or Irf2−/− (red) P14 T cells (i.v.) on day 9 after tumor initiation.

Data are representative of at least two independent experiments. Error bars represent mean ± SEM. ** p<0.001, *** p< 0.0001. One-way ANOVA for multiple comparisons used for tumor growth kinetics.