Extended Data Fig. 8: PTGIR expressing T cells poorly control tumor growth.
From: The prostacyclin receptor PTGIR is a NRF2-dependent regulator of CD8+ T cell exhaustion
(a) Relative PTGIR peptide (EMGDLLAFR) levels (normalized to ACTN4) from WT CD8+ T cells transduced with either an empty vector control (EV), or PTGIR expressing plasmid ( + PTGIR), and Keap1-/- CD8+ T cells transduced with EV control (mean±SEM, n = 3). (b) Raw intensity levels of PTGIR peptides GFTQAIAPDSR and (c) EMGDLLAFR, and (d) α-actinin-4—or ACTN4—peptide LVSIGAEEIVDGNAK from engineered cells described in (a) (mean±SEM, n = 3). (e) Individual growth curves, displayed vertically, for B16-OVA melanoma tumor growth in mice that received adoptive transfer of either WT empty vector control (WT + EV), PTGIR-expressing (WT + PTGIR), Keap1-/- empty vector (Keap1-/- + EV) OT-I CD8+ T cells, or HBSS at 7 dpti (mean±SEM, n = 12/group). (f) Individual growth curves, displayed vertically, for B16-OVA melanoma tumor growth in mice that received adoptive transfer of WT sgScr + EV, Keap1-/- sgScr + EV, Keap1-/- sgNfe2l2 + EV, Keap1-/- sgNfe2l2 + PTGIR OT-I cells, or HBSS at 6 dpti (mean±SEM, n = 12-20/group). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
