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The costimulatory molecules B7-H3 and B7-H4 are overexpressed in a variety of human tumors and have been hypothesized as possible biomarkers and immunotherapeutic targets. Despite this potential, the predominating uncertainty about their functional implication in tumor–host interaction hampers their evaluation as a target for cancer therapy. By means of a highly physiologic, spontaneous tumor model in mice, we establish a causal link between B7-H3 and host tumor control and found B7-H4 to be redundant. Cancer Immunol Res; 3(8); 849–54. ©2015 AACR.

Supplementary Figure Legend

Supplementary Figure 1. Increased B7-H3 and B7-H4 protein expression in murine prostate tumors. Supplementary Figure 2. Higher abundance of neoplastic epithelium in the absence of B7-H3. Supplementary Figure 3. Comparable levels of serum testosterone and AR expression in TRAMP+/- wt and TRAMP+/- B7-H3-/- mice. Supplementary Figure 4. B7-H3 does not influence tumor cell proliferation in a cell-intrinsic manner. Supplementary Figure 5. Immunosuppressive environment in TRAMP+ tumors in the absence of B7-H3. Supplementary Figure 6. B7-H3 does not affect T-cell proliferation or NK or CD8+ T-cell function directly. Supplementary Figure 7. Percentages of FoxP3+ cells in control (brachial) and tumor-draining (periaortic) lymph nodes are the same in TRAMP+wt and TRAMP+B7-H3-/- mice. Supplementary Figure 8. Percentages of NK1.1+, CD8+, CD4+ and CD11c+ cells among TILs in TRAMP+wt and TRAMP+B7-H3-/- mice. Supplementary Figure 9. B7-H3 is expressed by tumor-infiltrating lymphocytes.