负载Her-2多肽的DCIK细胞对乳腺癌细胞杀伤作用研究

本文观察利用树突状细胞(DC)呈递肿瘤抗原(Her-2多肽)的特性提高DCIK细胞对乳腺癌细胞的杀伤活性。提取外周血来源的有核细胞诱导分离出细胞因子诱导的杀伤细胞(CIK)和树突状细胞(DC),DC负载Her-2多肽后和CIK细胞共培养产生DCIK细胞,并鉴定其HLA基因型。分析三株肿瘤细胞(MDA-MB-231、SK-BR-3、MCF-7)HLA基因型和Her-2蛋白表达情况。用细胞毒试验(CCK-8法)测定DCIK细胞的对三株Her2表达不同的乳腺癌细胞株的杀伤活性。结果表明DCIK细胞对MDA-MB-31、SK-BR-3、MCF-7的杀伤率(效靶比10:1)分别为50.38%±3.25%、52.19%±3.25%、47.09%±2.41%。而负载Her-2多肽的DCIK细胞对MDA-MB-231、SK-BR-3、MCF-7的杀伤率分别为76.30%±1.74%(P<0.001)、55.70%±3.05%(P=0.0143)、47.67%±2.40%(P=0.6972)。实验证明负载Her-2多肽的DCIK细胞能显著提高对Her-2( )的乳腺癌细胞的杀伤作用,为乳腺癌患者进行过继免疫治疗提供了理论依据。

THE CYTOTOXICITY OF Her-2 PULSED DCIKS AGAINST BREAST CANCER CELLS

To study DCIK co-culture system with Her-2 as the pulsing antigen peptide of DC and the cytotoxicity of DCIKs against the breast cancer cells, CIK and DC were first induced and isolated from human peripheral blood. CIK and DC pulsed with antigen Her-2 peptide were then co-cultured to prepare CIK-DC co-culture system (DCIK-P). Using DCIK-P as effect cells and breast tumor cells (MDA-MB-231, SK-BR-3, MCF-7) as target cells,the antigen-specicfic cytotox-icity of DCIK-P was analysed by cell viability and cytotoxicity assay. The killer activity of DCIKs against the MDA-MB-231, SK-BR-3 and MCF-7 is 50.38% +/- 3.25%, 52.19% +/- 3.25% and 47.09% +/- 2.41% respectively. The killer activity of DCIK-Ps against the MDA-MB-231, SK-BR-3 and MCF-7 is 76.30% +/- 1.74% (P < 0.001), 55.70% +/- 3.05% (P = 0.014) and 47.67% +/- 2.40% (P = 0.697) respectively. The killer activity of DCIK-P cells was greatly enhanced against Her-2(+) breast tumor cell strains. The present results can provide tumor immunological data and experimental techniques for the development of breast tumor treatment.