中文摘要：

目的比较HPV16型E7抗原CTL表位E711-20（YMLDLQPETF）与其修饰多肽配体APL（YLLDLQPEVT）诱发特异CTL免疫应答的能力和抗肿瘤免疫治疗的作用。观察F711-20如及其APL的小鼠TC-1细胞肿瘤免除率、存活时间与荷瘤小鼠的肿瘤体积变化，了解其预防和治疗效果。方法以E711-20及其修饰多肽配体（APL）免疫C57BL／6小鼠，测定免疫后小鼠脾淋巴细胞的增殖指数；用LDH释放试验检测免疫后小鼠脾淋巴细胞的CTL杀伤活性。结果脾细胞增殖实验中，3组增殖指数如下：IFA4-APL组2．42±0．38，IFA＋E711-20组1．68±0．32，IFA组1．07±0．22；CTL杀伤效应实验中，3组靶细胞溶破率（％）如下：IFA4-APL组54．21±0．12，IFA＋E711-20组62．33±0．46，IFA组0．88±0．07；IFA组肿瘤免除率为0，IFA＋E711-20组肿瘤免除率为40％，IFA＋APL组肿瘤免除率为80％；荷瘤小鼠中，对照组IFA肿瘤体积迅速增大，E711-20和APL组的肿瘤生长速度较慢。APL免疫诱导的小鼠脾淋巴细胞，其CTL杀伤活性和增殖能力强于E711-20；APL对TC-1肿瘤细胞的预防和治疗效果优于E711-20。结论APL诱导特异性抗肿瘤免疫应答的能力和抗肿瘤效果优于E711-20，可能为针对HPVl6E7抗原的肽疫苗分子设计提供理想的CTL表位。

英文摘要：

Objective To compare the immunogenicity of HPV16 native CTL epitope E711-20（YMLDLQPETY） with its APL （YLLDLQPEVT） in inducing specific antitumor efficacy and priming specific CTL immune response. C57BL/6 mice were immunized with E711-20 or the APL emulsified in IFA. The rate of tumor-free, survival time, and tumor volume change were observed, to investigate the therapeutic and prophylactic effects to TC-1 tumor. Methods The specific lysis of CTL obtained from mice immunized with E711-20 or APL targeting to TC-1 ceils and splenocytes proliferatioin ability induced by E711-20 or the APL in the presence of E711-20 were assessed. Results The proliferation indexes of 3 groups were 2.42 ± 0.38 （ IFA ＋ APL）, 1.68 ± 0.32 （ IFA ＋ E711-20 ）, 1.07 ± 0.22 （IFA） respectively. The lysis rates （ % ） of target cells were 54.21 ±0.12 （IFA ＋APL）, 62.33 ±0.46（IFA ＋ E711-20） , 0.88 ±0.07 （IFA）. The rates （%） of tumor-free were 0（ IFA）, 40（ IFA ＋ E711-20 ）, 80 （IFA ＋ APL）. The gross tumor volume developed rapidly, but slowly in the other 2 groups. The specific lysis of CTL targeting to TC-1 cells and splenocytes proliferatioin ability induced by APL were higher than that of E711-20. The therapeutic and prophylactic effect induced by APL were more obvious than E711-20. Conclusion APL has the superior immunogenicity compared with E711-20, and provided ideal CTL epitope for HPV16 peptide-based vaccine design possibly.