Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. STING expression in CD14+ monocytes and CD19+ B cells in PBMCs from healthy volunteers and patients with cancer.
  • Fig. S2. STING expression in CD8+ T cells of CD4cre+-STINGflox/flox mice.
  • Fig. S3. T cell development and homeostasis in the KO mice.
  • Fig. S4. Representative flow cytometry gating strategy of the cells isolated from the tumor of one mouse after transfer.
  • Fig. S5. The expression of TCF1 and the frequency of TCF1+Slamf6+ cells in PD-1+ or PD-1 tumor-infiltrating 2C-CD8+ T cells.
  • Fig. S6. The impact of TCF1 on maintaining CD8+ T cell stemness in vivo.
  • Fig. S7. The frequency and magnitude of TCF1 expression in IFNAR1+/− 2C-CD8+ T cells after transfer.
  • Fig. S8. Stimulated CD8+ T cells without the cGAS-STING cascade are still viable.
  • Fig. S9. Quantification of Tcf7 mRNA in CD8+ T cells upon stimulation.
  • Fig. S10. The effect of various quantities of IFN-β on regulating TCF1 expression in PD-1+CD44+CD8+ T cells from WT and cGAS−/− mice.
  • Fig. S11. The cGAS-STING cascade prevents the overactivation of CD8+ T cells.
  • Fig. S12. The rescue of TCF1 expression in cGAS-deficient CD8+ T cells by an Akt inhibitor but not by an mTOR inhibitor.
  • Fig. S13. The staining of cytosolic dsDNA and dsRNA in CD8+ T cells with or without DNase or RNase treatment.
  • Fig. S14. The gating strategy of TSCM and TEFF in CD8+ T cells from patients with cancer and healthy volunteers.
  • Fig. S15. The viability and STING phosphorylation of CD8+ T cells stimulated with a STING agonist.
  • Fig. S16. Schematic of proposed mechanism for the differentiation of stem cell–like CD8+ T cells mediated by the cGAS-STING pathway in T cell therapy.
  • Table S1. Studied patients.

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