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目的：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 ＣＤＳ＋ 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。
Objective: To explore the point mutation of recombinant vaccinia virus-induced anti-tumor immune response and B7 strengthen its role in providing experimental evidence for the use of recombinant antigen vaccine for tumor immunotherapy. Methods: CTL was induced by rVV-p53, a recombinant vaccinia virus expressing rVV-p53FL with p53 point mutation at 135 Cys → Tyr point mutation. Immune protection and therapeutic effect in tumor-bearing mice. Results: BALB / c mice were immunized with rVV-p53FL to induce CDS + T cell-specific CTLs. rVV-p53FL protects some mice from tumor cells. Treatment of tumor-bearing mice with rVV-p53FL significantly prolonged the mean survival of mice. Inoculation of rVV-B7 with rVV-p53FL in a 1: 1 ratio can partially potentiate the therapeutic effect of rvv-p53FL. CONCLUSION: The overexpressed mutant P53 protein in tumor cells can be used as the target antigen for CTL recognition and attack. Using the mutant P53 protein as a tumor antigen vaccine can induce the body to produce p53-specific anti-tumor immune response. Costimulatory molecule B7 enhances tumor antigen-induced anti-tumor immune response.