Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. MC38/CD86 tumor growth inhibition is immune cell dependent and potentiated by therapeutic anti–PD-1.
  • Fig. S2. Localization of PD-1/PD-L1 and CD28 at the immunological synapse in the presence of PD-1/PD-L1 mAbs.
  • Fig. S3. PSMAxCD28 bispecific and PD-1 or PD-L1 blockade promote T cell activation in vitro.
  • Fig. S4. MUC16xCD28, but not a MUC16xCD27 T cell binding control, promotes T cell activation.
  • Fig. S5. SPR-Biacore sensorgrams for binding of human and murine CD28 to human and murine CD80 and CD86.
  • Fig. S6. PSMAxCD28 and PD-1 mAb combination increases the frequency of tumor-specific T cells.
  • Fig. S7. PSMAxCD28 cooperates with anti–PD-1 to induce intratumoral but not splenic or systemic cytokines.
  • Fig. S8. Expression of T cell activation markers used to determine CITRUS clusters shown in Fig. 3.
  • Fig. S9. Tumor antigen-specific (p15E+) CD8 T cell CITRUS analysis.
  • Fig. S10. EGFRxCD28 bispecific potentiates T cell activation only in the presence of TCR stimulation.
  • Fig. S11. A431 human xenograft tumor model.
  • Fig. S12. MFI data for CITRUS clusters shown in Fig. 4.
  • Fig. S13. PSMAxCD28 alone or in combination with PD-1 mAb does not induce cytokine in non–tumor-bearing mice, in contrast to CD28 superagonist.
  • Fig. S14. EGFRxCD28 alone or in combination with PD-1 mAb does not induce cytokines in human immune cell-engrafted STRG mice, in contrast to CD28 superagonist.
  • Table S1. SPR-Biacore kinetics.
  • Table S2. Measuring binding kinetics of human and mouse CD28/CD80/CD86 interactions using SPR.
  • Table S3. Histopathology, organ weights, body weight, and clinical pathology findings in cynomolgus monkeys.
  • References (7577)

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