Extended Data Fig. 10: Ptgir knockdown improves anti-viral CD8+ T cell responses and attenuates tumor growth.
From: The prostacyclin receptor PTGIR is a NRF2-dependent regulator of CD8+ T cell exhaustion
(a) Bar graph quantifying the number of control (shCtrl) and Ptgir knockdown (shPtgir) P14 donor cells in the spleen of LCMV CL13-infected mice at 8 dpi (mean±SEM, n = 4-5/sample). CD45.2 is a donor cell marker expressed by P14 T cells. (b) Bar graph of PD-1hi/TIM-3hi shCtrl- versus shPtgir-expressing P14 T cells from cells in (a). (c) Quantification of the percentage and number of polyfunctional (IFN-γ+/TNF-α+) PD-1hi shCtrl- versus shPtgir-expressing P14 T donor cells from LCMV CL13-infected mice at 8 dpi, and re-stimulated with gp33 peptide (1 μg/mL) in vitro (mean±SEM, n = 4-5/sample). (d) Individual growth curves, displayed vertically, for MC38-OVA tumors following adoptive transfer of OT-I CD8+ T cells expressing control (shCtrl) and Ptgir (shPtgir) shRNAs at 7 dpti. (e) Kaplan-Meier (KM) survival curves for time to tumor endpoint ( > 1500 mm3) for MC38-OVA tumors. (f) Individual growth curves, displayed vertically, for B16-OVA tumors following adoptive transfer of OT-I CD8+ T cells expressing control (shCtrl) and Ptgir (shPtgir) shRNAs at 7 dpti. (g) Kaplan-Meier (KM) survival curves for time to tumor endpoint ( > 1500 mm3) for B16-OVA tumors. **P < 0.01.
