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目的:探讨不同形式的肝癌抗原修饰的树突状细胞(DC)的抑瘤功能。方法:分别用肝癌H22冻融抗原、H22小分子抗原肽和Hsp70-H22抗原肽复合物修饰DC;用MTT比色法分析DC激活的CTL对H22细胞的杀伤能力,并用RT PCR法测定脾脏T细胞中IFN-γmRNA的表达水平;用不同修饰的DC免疫小鼠,观察其对H22肝癌的生长抑制作用。结果:单独的H22肝癌抗原肽修饰的DC不能激活CTL。Hsp70-H22肽复合物修饰的DC激活CTL的能力强于H22肝癌冻融抗原修饰的DC,对H22细胞的杀伤率分别为 47. 3%和 18. 3%。各组T细胞中IFN-γ表达水平的变化与杀伤率的变化相一致。用H22肝癌冻融抗原和Hsp70 -H22肽复合物修饰的DC免疫小鼠后,均可抑制H22细胞生长,但后者的抑制作用更强,成瘤率仅 40%。其他各组的成瘤率均为100%。结论:Hsp70-H22肽复合物是一种DC的强致敏物,可通过激活CTL、诱导CD4+T细胞分化成Th1型细胞而参与肝癌的免疫排斥。
Objective: To investigate the anti-tumor function of dendritic cells (DCs) modified with different forms of HCC. Methods: DCs were modified with H22 freeze-thaw antigen, H22 small molecule antigen peptide and Hsp70-H22 antigen peptide complex, respectively. The cytotoxicity of DC-activated CTL to H22 cells was analyzed by MTT colorimetric assay. The expression of IFN-γmRNA in the cells was observed. The mice with different modified DCs were immunized to observe the growth inhibition effect on H22 hepatocarcinoma. Results: DCs modified with H22 hepatoma antigen peptide alone failed to activate CTL. 3% 和 18. 3%. Hsp70-H22 peptide complex modified DC activated CTL ability H22 hepatocellular carcinoma freeze-thaw antigen modified DC, H22 cell killing rates were 47.3% and 18.3%. The changes of IFN-γexpression levels in T cells in each group were consistent with the change of killing rate. The growth of H22 cells was inhibited by H22 hepatocarcinoma cells modified with freeze-thaw antigen and Hsp70-H22 peptide complex, but the inhibition was stronger and the rate of tumor formation was only 40%. The tumor formation rates of other groups were 100%. Conclusion: The Hsp70-H22 peptide complex is a strong DC sensitizer that can participate in the immune rejection of HCC by activating CTL and inducing CD4 + T cells to differentiate into Th1 type cells.