探索点突变p53重组痘苗病毒诱导的抗瘤免疫反应及B7对其加强作用，为重组抗原疫苗用于肿瘤免疫治疗提供实验依据。方法： 选择人135位Cys→Tyr点突变p53作为肿瘤相关抗原模型，观察以表达该点突变p53的重组痘苗病毒rVV-p53FL单独和联合表达B7的重组痘苗病毒rVV-B7所诱导的CTL及对荷瘤小鼠的免疫保护和治疗作用。结果:以rVV-p53FL经静脉免疫BALB/c小鼠能够诱导以CD8+ T细胞为主的特异性CTL。rVV-p53FL能够保护部分小鼠免遭肿瘤细胞的攻击。以rVV-p53FL治疗荷瘤小鼠，可显著延长小鼠平均存活期。rVV-B7与 rVV-p53FL以1∶1的比例混合接种可部分加强rVV-p53FL的治疗作用。结论： 肿瘤细胞内过度表达的突变P53蛋白可作为CTL 识别和攻击的靶抗原，以突变P53蛋白作为肿瘤抗原的疫苗可诱导机体产生p53特异性的抗瘤免疫反应。共刺激分子B7可加强肿瘤抗原诱导的抗瘤免疫反应。

This study was aimed to explore antitumorresponses induced by recombinant vaccinia viruses expressing a point mutant p53 (rVV-p53FL) and enhancive effects of recombinant vaccinia viruses expressing costimulatory molecule B7 (rVV-B7). Methods: A 135 Cys to Tyr point mutant p53 protein was used as the model of tumor associated antigen. rVV-p53FL and rVV-B7 were used as vaccines to test their induction of CTLs and antitumor immunity. Results: Immunization BABL/c mice with rVV-p53FL could elicited specific CD8 + CTLs that could effecively lyse P815-mp53 cells, a transfectant of the murine P815 mastocytoma containing the mutant p53 gene. Treatment with rVV-p53FL could survive a part of mice challenged with 1×10 6 P815-mp53. Treatment with rVV-p53FL could significantly prolong survival of tumor-bearing mice. Admixture at 1∶1 ratio of rVV-p53FL and rVV-B7 could enhance therapeutic antitumor effects of rVV-p53FL. Conclusion: Mutant P53 over-expressed in tumor cells can render cells targets for specific CTLs generated by immunization with mutant P53 protein based vaccine. Costimulatory molecule B7 can enhance tumor-associated antigen inducing antitumor responses.