Supplementary Materials

Supplementary Material for:

Disruption of CXCR2-Mediated MDSC Tumor Trafficking Enhances Anti-PD1 Efficacy

Steven L. Highfill, Yongzhi Cui, Amber J. Giles, Jillian P. Smith, Hua Zhang, Elizabeth Morse, Rosandra N. Kaplan, Crystal L. Mackall*

*Corresponding author. E-mail: cm35c@nih.gov

Published 21 May 2014, Sci. Transl. Med. 6, 237ra67 (2014)
DOI: 10.1126/scitranslmed.3007974

This PDF file includes:

  • Fig. S1. Therapeutic efficacy of PD1 blockade therapy is lost in mice lacking T cells.
  • Fig. S2. M3-9-M RMS cells produce cytokines capable of inducing MDSCs.
  • Fig. S3. Morphology of tumor-resident CD11b+Ly6Ghi and CD11b+Ly6Chi cells is the same when obtained from wild-type B6 versus CXCR2 KO hosts.
  • Fig. S4. Regulatory T cell frequency is not increased in tumor-bearing hosts.
  • Fig. S5. RMS cells do not produce other CXCR2 ligands CXCL5 and CXCL7.
  • Fig. S6. Splenic MDSC migration toward tumor cells in vitro is partially dependent on CXCL1/CXCL2/CXCR2.
  • Fig. S7. CXCR2−/− MDSCs are increased in the spleens and peripheral blood of RMS tumor–bearing hosts.
  • Fig. S8. Pediatric patient sample evaluation based on tumor histotype.
  • Fig. S9. No difference in PD-L1 expression on wild-type versus CXCR2−/− MDSCs.
  • Fig. S10. The effectiveness of PD1 checkpoint blockade on 76-9 RMS is enhanced by anti-CXCR2 mAbs.
  • Fig. S11. Unfractionated peripheral blood samples from sarcoma patients contain higher frequency of HLA-DRCD11b+CD15+CXCR2+ MDSCs than normal patients.
  • Fig. S12. Flow cytometry gating strategy for Fig. 1B.
  • Fig. S13. Flow cytometry gating strategy for Fig. 1 (E and F).

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