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. Author manuscript; available in PMC: 2020 Aug 8.
Published in final edited form as: Cell. 2019 Aug 8;178(4):933–948.e14. doi: 10.1016/j.cell.2019.07.019

Figure 6. Activated bystander T cells support and Tregs inhibit NK/ILC1-dependent response after blocking tumor IFNG signaling.

Figure 6.

A) OT-1 mice bearing Res 499 tumors with combined IFNGR and B2M KO were treated with anti-CTLA4 with or without intratumoral injection of OVA peptide. Wild type mice with or without CD8 T cell depletion were used as comparison. B) Tumor infiltration by CD8 T cells and NK/ILC1s and C) growth of Res 499 IFNGR + B2M KO tumors after anti-CTLA4 (95% confidence interval in grey). D) Proliferation status of Tregs and other intratumoral immune cells in control (WT) or Res 499 IFNGR KO tumors measured by average expression of Ki67 and Top2a. E) Tumor growth of Res 499 IFNGR KO tumors implanted into wild type or FoxP3-DTR mice treated with anti-CTLA4 or diptheria toxin (DT). F) Survival of mice bearing CT26 tumors with IFNGR +/− B2M KO after treatment with anti-PD1 or anti-CTLA4. For all groups, n=5. G) Top predictive features from a random forest model (and confirmed by lasso regression) for how the proportion of different intratumoral immune cells (x-axis) predicts the proportion of activated NK cells in human melanoma tumors (y-axis). Standard error is in yellow. See also Figure S6.