Supplementary Materials

The PDF file includes:

  • Fig. S1. STING-deficient recipients exhibit greater lymph node cellularity versus WT recipients.
  • Fig. S2. Cohousing recipient WT and STING-deficient mice does not alter reduced GVHD in STING−/− recipients after MHC-matched aHSCT.
  • Fig. S3. C3H.SW donor T cells cause limited intestinal GVHD.
  • Fig. S4. Donor immune cell reconstitution is similar between B6-WT and B6-STING−/− syngeneic recipients.
  • Fig. S5. Altering the time and severity of conditioning abrogates the effect of STING deficiency on GVHD after MHC-matched HSCT.
  • Fig. S6. STING-deficient recipients also develop reduced GVHD after transplant of 10-fold higher numbers of T cells.
  • Fig. S7. Further activation of STING with a small-molecule agonist at the time of MHC-matched aHSCT exacerbates early GVHD-induced weight loss.
  • Fig. S8. B6N-STINGHAQ/HAQ peritoneal cells have markedly reduced responsiveness to STING ligands.
  • Fig. S9. CD4+ T cells are not sufficient for exacerbated MHC-mismatched GVHD in STING-deficient recipients.
  • Fig. S10. Fewer STING-deficient APCs are apoptotic early after aHSCT.
  • Fig. S11. Donor regulatory T cells are activated more efficiently in STING-deficient recipients.
  • Fig. S12. Recipient nonhematopoietic STING reduces the survival of recipient APCs early after aHSCT.
  • Fig. S13. Gating strategy for the identification of live cells, singlets, and donor T cells to examine activation phenotype.
  • Table S1. Antibodies and qPCR primers.

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Other Supplementary Material for this manuscript includes the following: