Science Immunology

Supplementary Materials

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  • Fig. S1. Comparable CD274 expression between EGFR-mutated and EGFR wild-type NSCLC cell lines after IFN-γ treatment.
  • Fig. S2. The expression of CD274 and other immune-related genes and tumor mutation burden in EGFR-mutated and wild-type LUADs in our cohort and TCGA data.
  • Fig. S3. Representative t-distributed stochastic neighbor embedding (tSNE) plots for 34 immune-related markers in patients with EGFR-mutated and wild-type surgically resected LUADs with CyTOF assays.
  • Fig. S4. Graphical summary schema of two different mechanisms for Treg infiltration into the TME of EGFR-mutated and wild-type LUADs.
  • Fig. S5. Relationships between clinical features (smoking status, tumor size, and clinical stage) and CD8+ T cell or Treg infiltration.
  • Fig. S6. The comparable infiltration of TAMs, MDSCs, and DCs in the TME of EGFR-mutated and wild-type LUADs with multifluorescent IHC.
  • Fig. S7. GSEA of the differences in activated EGFR and inhibited EGFR signals in three NSCLC cell lines in microarray analyses.
  • Fig. S8. CCL5 expression in EGFR-mutated and wild-type NSCLC cell lines treated with erlotinib.
  • Fig. S9. CXCL10, CCL5, and CCL22 expression and EGFR downstream signals in EGFR-mutated and wild-type NSCLC cell lines treated with a third-generation EGFR tyrosine kinase inhibitor, osimertinib.
  • Fig. S10. EGFR expression by CD8+ T cells and Tregs in PBMCs and their sensitivity to erlotinib.
  • Fig. S11. CXCL10 and CCL22 expression in patients with EGFR-mutated LUADs before and after EGFR tyrosine kinase inhibitor treatment.
  • Fig. S12. Antitumor effects by the combination of erlotinib and anti–PD-1 mAb in single clones of EGFR mutant (exon 19 deletion)–transfected MC-38.
  • Fig. S13. In vitro proliferation and sensitivity to erlotinib in mock-transfected, wild-type, and EGFR mutant (exon 19 deletion)–transfected MC-38 cell lines.
  • Fig. S14. Changes in CD8+ T cell and Treg infiltration in MC-39ex19del tumors after CXCL10 or CCL22 blockade administration, respectively.
  • Fig. S15. Antitumor effects by the combination of erlotinib and anti–PD-1 mAb in MC-38ex19del tumors under Treg-depleted conditions induced by anti-CD25 mAb.
  • Fig. S16. The changes in other chemokines induced by EGFR signaling in microarray analysis.
  • Table S1. Summary of patients with LUAD who received surgery.
  • Table S2. Summary of patients with LUAD who received EGFR tyrosine kinase inhibitor therapy.
  • Table S3. Summary of antibodies used in the IHC.
  • Table S4. Summary of antibodies used in the CyTOF analyses.
  • Table S5. Summary of antibodies used in the flow cytometry analyses.
  • Table S6. Primers used in qRT-PCR.
  • Table S7. Summary of antibodies used in Western blotting.

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