Fig. 1

High glucose may inhibit T cell function in the tumor microenvironment by enhancing PD-L1 expression in pancreatic cancer cells. A KEGG pathway enrichment analysis of 146 PDAC samples from TCGA. Bubble charts depicting pathway changes in PDAC samples complicated with diabetes (n = 38) compared to samples without diabetes (n = 108). B Single cell transcriptome data of 24 pancreatic cancer tumors from a public cohort were analyzed (CRA001160). Bubble charts depicting differential genes related to immune checkpoints and killing function between CD8⁺ T cells in PDAC samples complicated with diabetes (n = 10) and samples without diabetes (n = 14). C Single cell transcriptome data of 24 pancreatic cancer tumors from a public cohort were analyzed (CRA001160). Bubble charts depicting differential genes related to immune checkpoints ligands between tumor epithelial cells in PDAC samples complicated with diabetes (n = 10) and samples without diabetes (n = 14). D Barplot depicting glucose content of tumor tissue in euglycemic (n = 8) and hyperglycemic mice (n = 8). E Flow cytometry analysis of the infiltration of immune effectors (CD45⁺ cells, CD3⁺ T cells, CD3⁺ CD4⁺ T cells, Tregs, CD3⁺ CD8⁺ T cells, IFN-γ⁺ CD8⁺ T cells, PD-1⁺ CD8⁺ T cells, KI67⁺ CD8⁺ T cells, DC, MDSC, Macrophages, M1-type macrophages, M2-type macrophages) in the orthotopic tumors of hyperglycemia (n = 8) and euglycemia mice (n = 8). F Immunohistochemical staining to evaluate the distribution and level of PD-L1 expression in the orthotopic tumors of hyperglycemia and euglycemia mice