ALA-PDT能有效治疗皮肤鳞状细胞癌（SCC），治疗后出现强烈的炎症反应，瘤体局部可见大量炎症细胞浸润，但其机制仍不清楚。本课题组前期应用表达谱芯片和生物信息学对紫外线诱导的小鼠皮肤鳞癌样本进行分析，发现ALA-PDT治疗后瘤体局部CCL8 的表达显著上调，同时，其相关受体表达亦显著升高，提示ALA-PDT可能通过上调CCL8的表达趋化免疫细胞在肿瘤治疗部位聚集，打破肿瘤微环境，启动抗肿瘤免疫反应。为验证以上假设，本课题拟进一步应用临床样本、小鼠皮肤鳞癌模型，体外采用原代肿瘤细胞与巨噬细胞共培养等体系从体内、细胞与分子水平，探讨CCL8在ALA-PDT治疗SCC中的作用及机制，为ALA-PDT增敏剂的研发设计提供靶点，为临床应用ALA-PDT治疗皮肤鳞癌提理论基础。

Squamous cell carcinoma (SCC) was treated by ALA-photodynamic therapy (ALA-PDT) and achieved satisfied outcomes. It was showed strong inflammatory after topical ALA-PDT, with a large number of immune cells in the tumor tissues after treatment, however, the mechanism behind this process remains unclear. According to our previous study, we analyzed ultraviolet induced mouse SCC model samples treated by ALA-PDT via gene chip and bioinformatics, and found C-C motif ligand 8 (CCL8) and its receptors were upregulated significantly after ALA-PDT. We hypothesized that CCL8 is very important for suppressing growth of SCC by ALA-PDT via recruiting immune cells to tumor lesions. In order to confirm the hypothesis, we will further explore the effect and the mechanism of CCL8 induced by ALA-PDT. Clinical samples, mouse SCC models and the system of coculture of primary tumor cells and macrophages will be used to develop further experiments. An insight view into the mechanism can throw lights on a target spot on the development of ALA-PDT sensitizer, and provide new theoretical evidence on the clinical effect.