Science Immunology

Supplementary Materials

The PDF file includes:

  • Fig. S1. Epitope-specific expression of CD103 and PD-1 on TRM cells.
  • Fig. S2. Epitope-specific expression of inhibitory receptors on TRM cells.
  • Fig. S3. Exhausted-like TRM cells are present in the X31 influenza model.
  • Fig. S4. Exhausted-like TRM cells respond effectively to recall in situ.
  • Fig. S5. Cognate peptide inoculation directly promotes PD-1 expression on PA224–233 TRM cells.
  • Fig. S6. Nur77 (Nr4a1) is required for the induction and/or maintenance of exhausted-like TRM cells.
  • Fig. S7. Limiting NP antigen dose decreases the exhaustion phenotype.
  • Fig. S8. TCR signaling and inhibitor receptor expression on exhausted-like TRM cells are lost 4 months after infection.
  • Fig. S9. Persistent MHC-I engagement maintains exhausted-like TRM phenotypes and cells.
  • Fig. S10. NP366–374 TRM cells, PD-1 expression, and heterologous protection are lost over time.
  • Fig. S11. Continuous CD28 signaling is required for the maintenance of NP366–374 TRM cells.
  • Fig. S12. PD-L1 blockade promotes exhausted-like TRM cell survival and CD103 expression.
  • Fig. S13. PD-L1 blockade promotes cytokine production of exhausted-like TRM cells to antigenic restimulation.
  • Fig. S14. PD-L1 blockade promotes CD103 expression.
  • Fig. S15. B7 signaling is required for the effects of PD-L1 blockade.
  • Fig. S16. PD-L1 blockade promotes heterologous immunity and causes tissue pathology.
  • Fig. S17. CD8 T cells are responsible for the development of tissue pathology after α-PD-L1 blockade.
  • Fig. S18. ILD lungs exhibit elevated PD-1, CD103, and TIM-3 expression.

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Other Supplementary Material for this manuscript includes the following:

  • Table S1 (Microsoft Excel format). Raw data.

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