Cetuxi-mAb联合NK细胞治疗EGFR+表达肿瘤具有协同抑制效应，肿瘤杀伤效果良好，是近几年肿瘤非手术治疗领域备受关注的热点。目前，影响Cetuxi-mAb联合NK杀伤EGFR+结直肠癌细胞的机制尚未明了。有证据提示，Cetuxi-mAb和NK细胞协同抗肿瘤过程中，可能会受到NK细胞Fc受体（FcγRIIIa）亲和力以及肿瘤细胞上NK细胞凝集素类受体配体（NKG2DLs）的影响。肿瘤细胞上的NKG2DL与NK细胞的NKG2D结合后，使NK细胞激活，发挥识别和杀伤肿瘤细胞的作用。本项目拟通过体外细胞共培养实验；EGFR+细胞株裸鼠移植瘤模型建立和干预两个层次的研究，探索NK细胞Fc受体（FcγRIIIa）基因型及活化轴NKG2D/NKG2DLs表达与其杀伤肿瘤细胞活性的关系，发现其杀伤作用的调控因素，为研究抗EGFR单抗等靶向药物联合NK细胞生物治疗方案的优化和改良提供理论基础。

The combination of molecular targeted agents named cetuxi-mAb with NK cell immunotherapy comes out the focus of attention in treatment of oncology in recent years. Throughout the previous research, cetuxi-mAb combined NK has a co-suppression effect to EGFR+ Colorectal cancer cells in vitro enhancing their killing effect on EGFR+ tumor cells. The factors influencing the killing effect of cetuxi-mAb combined with NK are poorly elucidated. There is evidence suggesting that cetuxi-mAb and NK cells may be affected by the affinity of Fc receptor (Fc) of NK receptor (RIIIa) as well as NKG2DLs on the tumor cells in the process of synergistic anti-tumor. The study combined with co-culture cells trials in vitro, establishment of nude mice transplantation tumor model for EGFR+ cells and clinical verification test, exploits of Fc receptor (Fc gamma RIIIa) gene type of NK cell and the relationship between expression of NKG2D/NKG2DLs which is the.activation axis of NK cells and the anti-tumor activity of cetuxi-mAb combined with NK cell. It aims to discuss the regulation factors of NK combined cetuxi-mAb against EGFR+ tumor cells, which provides theoretical basis for optimization and improvement of clinical protocols about the biological treatment of anti-EGFR monoclonal antibody (molecular targeted drugs) combined with NK cells.