程序性死亡配体-1（PD-1）通过抑制免疫细胞功能在免疫逃脱、肿瘤发生和发展中发挥重要作用。然而，PD1在子宫体内膜癌（UCEC）中的预后价值及其对肿瘤微环境的影响还有待进一步探讨。本研究从GEPIA、TIMER和TCGA数据库中检索转录数据集。使用"edgeR"软件包，鉴定PD1高组和PD1低组之间有差异的基因（DEGs）。进行基因集富集分析（GSEA），以识别在UCEC中PD1高组和PD1低组之间发挥作用的潜在通路。使用基因相关性分析进一步确认PD1表达与T细胞相关基因的关联。利用Cytoscape软件在DEGs中识别中心基因。进行Kaplan-Meier分析，验证中心基因的预后价值。描述和分析了基于PD1水平的UCEC患者的突变特征。我们发现，在GEPIA和TCGA数据库的队列中，UCEC肿瘤组织中PD1基因的转录表达明显增加。PD1表达与与T细胞受体信号通路和原发性免疫缺陷相关的基因标志物呈负相关。GSEA证实PD1表达与与T细胞受体信号通路相关的基因标志物呈负相关。与PD1表达呈显著正相关的T细胞受体复合物相关基因包括ZAP70、TRAC、CD3D、CD3E、CD8A、TRBC2、TRBV28和CD247。Kaplan-Meier OS分析结果表明，PD1、TIGIT、FASLG、ICOS和TNFRSF9是UCEC患者的保护因子。低表达组的前5个突变基因包括PTEN（56%）、PIK3CA（43%）、TP53（41%）、TTN（39%）和ARID1A（37%）。PD1高组中具有更高突变比例的基因是PTEN（67%）、TTN（62%）、PIK3CA（53%）、ARID1A（52%）和MUC16（12%）。PD1过表达型UCEC患者的预后比PD1低组差，这是由于PD1基因参与了T细胞受体信号通路。本研究为针对PD1的靶向治疗提供了进一步的理论基础和参考依据。

Programmed death 1 (PD-1) plays an important role in the immune escape, occurrence and development of tumors by inhibiting the function of immune cells. However, its prognostic value in uterine corpus endometrial carcinoma (UCEC) and its impact on the tumor microenvironment remain to be further explored. Transcriptional datasets were retrieved from the GEPIA, TIMER and TCGA databases. "edgeR" package was used for the identification of differentially expressed genes (DEGs) between two groups of patients (PD1-high and PD1-low group). Gene set enrichment analysis (GSEA) was performed to identify underlying pathways between betweenPD1-high and PD1-low groups functioning in UCEC. Gene Correlation Analysis was used to further confirm the associations of PD1 expression with T-cell-related genes. Cytoscape software was used to identify hub genes in DEGs. Kaplan-Meier analysis was performed to validate the prognostic value of hub genes. Mutational characteristics of UCEC patients according to PD1 levels were depicted and analyzed. We found that the transcriptional expression of the PD1 gene in UCEC tumor tissues markedly increased in cohorts from the GEPIA and TCGA databases. PD1 expression was negatively correlated with gene signatures associated with the T-cell receptor signaling pathway and primary immunodeficiency. GESA confirmed that PD1 expression was negatively correlated with gene signatures associated with the T-cell receptor signaling pathway. T-cell receptor complex-related genes, ZAP70, TRAC, CD3D, CD3E, CD8A, TRBC2, TRBV28 and CD247, showed significant positive associations with PD1 expression. The results of the Kaplan-Meier OS analysis indicated that PD1, TIGIT, FASLG, ICOS and TNFRSF9 are the protective factor for patients with UCEC. The top 5 genes of mutations in the low expression group, included PTEN (56%), PIK3CA (43%), TP53 (41%), TTN (39%), and ARID1A (37%). The genes with a higher proportion of mutations in the PD1-high group are PTEN (67%), TTN (62%), PIK3CA (53%), ARID1A (52%), and MUC16 (12%). The prognosis of UCEC patients with PD1 overexpression phenotype is worse than that of the PD1 low group, which is due to the involvement of the PD1 gene in the T-cell receptor signaling pathway. This study provides a further theoretical basis and reference for targeted therapy against PD1.