Fig. 5. PTGIR is enriched in CD8 TIL and its expression correlates with poor tumor control.

(A) Correlation between NRF2 activity and Ptgir expression in CD8 T cell subsets. Relative Ptgir mRNA expression (Log₂ fold-change) versus NRF2 pathway enrichment scores (NFE2L2.V2) in CD8 T cells from Listeria monocytogenes infection (Tn, Teff, and Tmem) or CD8 TIL isolated from early (<21 days) versus late (>21 days) stage liver tumors (data from (24)). Expression values were normalized to Teff cells. Linear regression indicates goodness of fit (R²=0.92). (B) Relative PTGIR protein levels (normalized to ACTN4) in Keap1^−/− CD8 T cells following CRISPR/Cas9 gene editing using sgRNAs targeting Ptgir (sgPtgir) or non-targeting control (sgScr) (mean±SEM, n=3). (C) B16-OVA melanoma tumor growth in mice that received adoptive transfer of control (sgScr) or PTGIR-deleted (sgPtgir) Keap1^−/− OT-I CD8 T cells at 7 dpti (mean±SEM, n=15–17). (D) Relative PTGIR protein expression (normalized to ACTN4) in WT OT-I T cells following transduction with empty vector (CTRL) or PTGIR-expressing (PTGIR OE) retroviral vector (mean±SEM, n=3). (E) B16-OVA melanoma tumor growth in mice that received adoptive transfer of control (CTRL) or PTGIR-expressing (PTGIR OE) WT OT-I cells at 7 dpti (mean±SEM, n=8). **P<0.01, ***P<0.001, ****P<0.0001.