Science Immunology

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  • Fig. S1. Mice with experimental liver metastasis have a normal liver metabolic function.
  • Fig. S2. Liver-mediated suppression of distant antitumor immunity requires adaptive immunity but not high tumor burden.
  • Fig. S3. Activation markers are decreased on effector CD4+ and CD8+ T cells but increased on Tregs in mice with experimental liver metastasis.
  • Fig. S4. The percentage and number of Tregs and tetramer+ CD8+ T cells are similar in distant tumors.
  • Fig. S5. Experimental liver metastasis mediated suppression in the B16F10 tumor model.
  • Fig. S6. KSP tetramer specifically stains MC38 tumor–targeted CD8+ T cells.
  • Fig. S7. Suppression of distant CD8+ T cells is liver mediated and tumor antigen specific.
  • Fig. S8. Foxp3-DTR mouse model schema.
  • Fig. S9. DT induces profound Treg depletion in the blood and the SQ tumor of treated Foxp3-DTR mice.
  • Fig. S10. Combination therapy with Treg-depleting anti–CTLA-4 and anti–PD-1 antibodies overcomes experimental liver metastasis immune suppression.
  • Fig. S11. Clustering of tumor-infiltrating immune cell subsets using scRNA-seq.
  • Fig. S12. Differential gene expression in distant MDSCs driven by the presence of liver tumor.
  • Fig. S13. Liver tumor–mediated suppression is associated with distant increase in CD11b+ monocyte populations.
  • Fig. S14. Increase in distant tolerogenic MDSCs is anatomically unique to liver tumor.
  • Fig. S15. Treg or MDSC depletion can enhance tumor rejection in mice with experimental liver metastasis.
  • Fig. S16. Treg-depleting versus nondepleting anti–CTLA-4 antibody in combination with anti–PD-1 treatment in experimental liver metastasis.

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Other Supplementary Material for this manuscript includes the following: