由于低手术切除率和较差临床预后，针对胰腺癌的抗肿瘤免疫研究已成为关注热点。我们在前期研究中初步证实，胰腺癌组织中调节性T淋巴细胞（Treg细胞）浸润水平与肿瘤远处转移程度呈正相关，细胞共培养结合label-free定量及质谱分析技术发现，来源于Treg细胞的IL-10可诱导胰腺癌细胞发生上皮间质转化（EMT）。EMT是恶性肿瘤发生侵袭转移的关键事件。本项目拟利用人胰腺癌细胞系、临床胰腺癌标本和裸鼠原位模型，从体内外两方面证实Treg细胞诱导胰腺癌发生EMT导致肿瘤远处转移；采用启动子分析、小RNA干扰、染色质免疫共沉淀等方法，阐释IL-10-IL10R旁分泌通路可能介导上述过程的分子调控机制；并通过动物实验观察靶向干扰IL-10-IL10R旁分泌通路对抑制胰腺癌远处转移的作用，从而为有效改善胰腺癌诊疗处理和预后提供理论依据和实践基础

Due to the low resection rate and poor clinical prognosis, emerging studies have focused on antitumor immunity in pancreatic carcinomas. In our previous research, we observed that regulatory T lymphocyte (Treg cells) density in primary tumor tissue in patients with pancreatic cancer correlates with lymph node metastasis. Interleukin-10 derived from co-clutureTreg cells induced epithelial-mesenchymal transition (EMT), which is a key event during tumor metastasis, in pancreatic cancer cells. Here, we attempt to reveal the critical role of Treg cells in development of EMT in pancreatic cancers both in vitro and in vivo. Utilizing promoter analysis, small RNA interference and ChIP-PCR, we aim to clarify the involvement of the paracrine IL-10-IL10R axis during this process. Furthermore, we try to determine whether targeting the IL-10-IL10R axis in vivo represents an effective approach to prevent distant metastasis in pancreatic cancers. Therefore, further support of this program would provide theoretical basis and experimental evidence for improvement of pancreatic carcinoma treatment and prognosis.