Fig. 6

Overexpression of PTRH1 rescued T cell function from high glucose induced inhibiting effect of pancreatic cancer cells A Flow cytometry analysis of IFN-γ production of CD8⁺ T cells when cocultured with differentially treated SW1990 cells (5.5 mM concentration glucose, 25 mM concentration glucose, 25 mM concentration glucose + PTRH1 overexpression). B Experimental scheme and the details of experimental intervention in immune-competent C57BL/6 mice model (eight different treatment group with 5 mice per group). C The alterations in blood glucose levels after STZ treatment or fresh sodium citrate buffer as control in the mouse model. Blood was collected from mouse tails daily for the first 5 days after administration to measure blood glucose levels. Blood glucose was measured every 3 days thereafter until day 23. D Representative pictures and Box plot of the orthotopic tumors in immune-competent C57BL/6 mice in different groups. The pancreatic cancer cells were injected into the tail of the pancreas of mice and the tumors were harvested 3 weeks later. E Immunohistochemical staining to evaluate the distribution and level of PTRH1 and PD-L1 expression in the orthotopic tumors in immune-competent C57BL/6 mice in different groups. F Flow cytometry analysis of the proportion of infiltrated immune effectors (CD45⁺ cells, CD3⁺ T cells, Tregs, CD3⁺ CD8⁺ T cells, IFN-γ⁺ CD8⁺ T cells, PD-1⁺ CD8⁺ T cells, KI67⁺ CD8⁺ T cells) in the orthotopic tumors in immune-competent C57BL/6 mice in different groups. G Work model depicting the mechanism underlying the regulation on PD-L1 by high glucose and the changes of immune landscape in pancreatic TME. DC dendric cell, MDSC myeloid-derived suppressor cell, ns non-significant, *p  < 0.05, **p  < 0.01, ***p < 0.001