黑素瘤免疫过继治疗通常因难以诱导机体产生足够数量的能杀灭肿瘤的CD8(+)细胞毒性T淋巴细胞(CTL)、到达病灶部位的CTL活性受抑制、免疫应答持续时间短、难以控制辅助性细胞因子释放等原因导致抗瘤疗效有限。在前期工作基础上，我们拟利用新型生物组织工程支架作为CTL和辅助性细胞因子的载体来治疗黑素瘤：利用aAPC在体外扩增获得足够数量的黑素瘤抗原特异性CTL，然后将CTL和树突状细胞（DC）移植到生物支架上，同时在支架中包埋可活化DC的细胞因子GM-CSF以及肿瘤细胞裂解物，以促进CTL存活、增强其抗瘤作用、并降低负调控因子B7-H4的免疫抑制作用来减少肿瘤免疫逃逸效应；最后将生物支架植入黑素瘤病灶部位，研究其抗瘤效果及机制，为黑素瘤的临床免疫治疗进步，提供实验和理论依据。

Adoptive immunotherapy for malignant melanoma (MM) is challenged by generating sufficient number of activated CD8(+) cytoxic T lymphocytes (CTL) to kill tumor cells. Furthermore, the activity of effector CTLs is largely suppressed and their killing tumor effect is not sustained due to immune escape mechanism. In addition, as adoptive immunotherapy usually contains administration of cytokines, it's challenging to regulate cytokines release and optimize their therapeutic effect. Thus the outcome of this type of immunotherapy is unsatisfactory. Based on our previous work on tissue engineering scaffold, we propose to use scaffold as a delivering vehicle for cells and cytokines in this application for the treatment of malignant melanoma. We propose to use synthetic antigen presenting cell（aAPC) to induce enough quantity of melanoma antigen specific CTLs and then transfer CTLs and DCs to the scaffold. In the meantime, we propose to encapsulate cytokines such as granulocyte macrophage colony stimulating factor (GM-CSF)in the matrix of the scaffold. When used in combination with tumor lysate, GM-CSF could enhance DC antigen presenting effect and stimulating DC recruitment and proliferation, which in turn activates CTLs; in addition, GM-CSF is capable of down-regulating inhibitor B7-H4 expression to tilt the balance towards protective anti-tumor immunity. .The scaffold will be implanted at the tumor site and the outcome of the immunotherapy and the anti-tumor mechanism will be studied. Our strategy may provide theoretical and experimental proof that may contibute to future clinical treatment of malignant melanoma.