肿瘤的发生是内在的遗传不稳定性与外因包括免疫系统共同作用的结果。树突状细胞(DC)是包含多个亚群的异质性群体，是功能最强的专职抗原递呈细胞, 处于启动和调控免疫反应的中心地位。虽然获得性免疫在肿瘤的发生发展中扮演重要角色，但DC及其亚群在其中的作用却不十分清楚。我们的预实验发现致癌剂处理的引流淋巴结DC亚群在不同时间点的活化状态不一致，并鉴于DC调控免疫反应的中心作用，本课题组将以化学致癌剂为模型，以研究DC亚群在致癌剂诱导肿瘤的发生发展过程中对获得性免疫的调控作用和机理为核心科学问题，以现代免疫学方法结合转基因和基因敲除小鼠为模型的实验平台，研究DC亚群在肿瘤进展各阶段的功能, 阐明它们是如何分工、 合作进而调控肿瘤免疫反应的, 以明确它们在肿瘤"免疫编辑"中的作用及可能的机制。为阐明肿瘤免疫的机理做铺垫，为研制基于DC亚群的靶向性肿瘤治疗性药物和方法提供理论基础。

The combined effects of internal genetic instability and external factors including the dysfunction of immune system lead to the generation of the tumor. Dendritic cells (DC) that contains multiple subsets, are the most powerful professional antigen-presenting cells, and play a central role in the initiation and regulation of immune response. Although adaptive immunity plays an important role in tumor development, the role of DC and their subsets in tumorigenesis remain poorly understood. Our preliminary experiments found that the activity of DC subsets within the draining lymph nodes in different time points were different during tumorigenesis triggered by the carcinogen. Given the central role of DC in regulation of the immune response, we considered how DC subsets regulate adaptive immunity during tumorigenesis caused by carcinogen as the core scientific issues. Using modern immunology experimental techniques combined with transgenic and gene knock out mice, the project aims to investigate the division of labor, cooperation between DC subsets in modulating tumor immune response. We try to clarify the role of DC subsets in cancer immunoediting as well as their mechanisms. This study will help to elucidate the mechanism of anti-tumor immunity, and provide a theoretical basis for targeted cancer therapy by using DC subsets in the future.