目的 探讨牙龈卟啉单胞菌 (Pg) 感染对食管癌细胞免疫逃逸的影响以及 YTHDF2 和 Fas 在这一调节机制中的作用。我们检测了有和没有 Pg 的食管鳞状细胞癌 (ESCC) 组织中 YTHDF2 和 Fas 蛋白的表达。使用免疫组织化学法检测感染，并使用蛋白质印迹法检测 Pg 感染的 KYSE150 细胞。通过免疫共沉淀 (Co-IP) 研究了 YTHDF2 和 Fas 之间的相互作用。检查慢病毒介导的 YTHDF2 敲低的 Pg 感染的 KYSE150 细胞中 YTHDF2、组织蛋白酶 B (CTSB)、Fas 和 FasL 蛋白表达水平的变化，并观察 E64（组织蛋白酶抑制剂）对这些蛋白的影响。 Pg感染和E64处理后，KYSE150细胞与人外周血单个核细胞（PBMC）共培养，流式细胞术检测T细胞相关效应分子的表达。Pg感染的ESCC组织和细胞显示YTHDF2显着增加表达并降低 Fas 表达。 Co-IP 的结果证明了 YTHDF2 和 Fas 之间的直接相互作用。在YTHDF2敲低的Pg感染的KYSE150细胞中，CTSB的表达显着降低，而Fas和FasL的表达显着增加。 E64处理KYSE150细胞后，CTSB的表达显着降低，但不影响YTHDF2的表达，并且Fas和FasL的表达明显增加。流式细胞术显示，Pg感染的KYSE150细胞与PBMC共培养时，Granzyme B和Ki67的表达显着降低，而PD-1的表达显着增强。Pg感染YTHDF2依赖性地调节Fas的表达，促进细胞的免疫逃逸。食管癌，从而促进癌症进展，提示YTHDF2在调节食管癌免疫逃逸中发挥关键作用。

To investigate the effect of Porphyromonas gingivalis (Pg) infection on immune escape of oesophageal cancer cells and the role of YTHDF2 and Fas in this regulatory mechanism.We examined YTHDF2 and Fas protein expressions in esophageal squamous cell carcinoma (ESCC) tissues with and without Pg infection using immunohistochemistry and in Pg-infected KYSE150 cells using Western blotting. The interaction between YTHDF2 and Fas was investigated by co-immunoprecipitation (Co-IP). Pg-infected KYSE150 cells with lentivirus-mediated YTHDF2 knockdown were examined for changes in expression levels of YTHDF2, cathepsin B (CTSB), Fas and FasL proteins, and the effect of E64 (a cathepsin inhibitor) on these proteins were observed. After Pg infection and E64 treatment, KYSE150 cells were co-cultured with human peripheral blood mononuclear cells (PBMCs), and the expressions of T cell-related effector molecules were detected by flow cytometry.ESCC tissues and cells with Pg infection showed significantly increased YTHDF2 expression and lowered Fas expression. The results of Co-IP demonstrated a direct interaction between YTHDF2 and Fas. In Pg-infected KYSE150 cells with YTHDF2 knockdown, the expression of CTSB was significantly reduced while Fas and FasL expressions were significantly increased. E64 treatment of KYSE150 cells significantly decreased the expression of CTSB without affecting YTHDF2 expression and obviously increased Fas and FasL expressions. Flow cytometry showed that in Pg-infected KYSE150 cells co-cultured with PBMCs, the expressions of Granzyme B and Ki67 were significantly decreased while PD-1 expression was significantly enhanced.Pg infection YTHDF2-dependently regulates the expression of Fas to facilitate immune escape of esophageal cancer and thus promoting cancer progression, suggesting the key role of YTHDF2 in regulating immune escape of esophageal cancer.