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目的 :应用转染有小鼠B7- 2基因片段的肝癌细胞 ,建立小鼠肝癌模型 ,观察小鼠肿瘤生长和消退情况 ,研究共刺激分子B7- 2对肿瘤的免疫治疗作用。方法 :建立BALB/c小鼠转B7- 2基因肝癌细胞株H2 2 /B7- 2 ,细胞计数法测定肿瘤细胞体外增殖能力 ;BALB/c鼠皮下接种H2 2 /B7- 2及野生型H2 2细胞H2 2 /Wt,以空载体转染细胞H2 2 /neo为对照 ,建立小鼠肝癌模型 ,观察小鼠成瘤期、荷瘤小鼠存活期及肿瘤结节大小 ;同源淋巴细胞肿瘤细胞混合培养 (MTLCs)后测定淋巴细胞增殖指数和CTLs活性 ,同时测定培养上清IL -2、IFNγ ,研究B7- 2分子的抗肿瘤免疫效果。结果 :细胞在体外增殖能力一致 (P =0 .782 ) ;当接种不同肿瘤细胞后 ,三组动物都发生肿瘤 ,接种H2 2 /B7- 2组肿瘤形成有迟发性 ,并在接种 18d后肿瘤都开始缩小 ,但最终不会完全消失 ;接种H2 2 /Wt和H2 2 /neo组动物肿瘤呈进行性生长。H2 2 /B7- 2在体外刺激淋巴细胞增殖和诱导CTLs的能力明显强于对照细胞 (P <0 .0 5 )。结论 :共刺激分子B7- 2能增强肝癌细胞的免疫原性 ,它在抗肿瘤早期发挥作用。用其治疗肝癌是有效的 ,但不能介导完全和长期的抗肿瘤效应。
OBJECTIVE: To establish a murine model of hepatocellular carcinoma (HCC) by transfecting hepatoma cells transfected with mouse B7-2 gene fragment and to observe the growth and regression of tumor in mice and to study the immunotherapeutic effect of costimulatory molecule B7-2 on tumor. Methods: The B7-2 hepatocarcinoma cell line H2 2 / B7-2 was established in BALB / c mice and the proliferation of tumor cells was determined by the cell counting method. The BALB / c mice were inoculated subcutaneously with H2 2 / B7-2 and wild-type H2 2 Cells H2 2 / Wt, the empty vector transfected cells H2 2 / neo as control, a mouse model of liver cancer was established to observe the mouse tumorigenicity, tumor-bearing mice survival and tumor nodule size; homologous lymphocyte tumor cells After mixed culture (MTLCs), the proliferation index of lymphocytes and the activity of CTLs were measured. The anti-tumor immunity effects of B7-2 were studied by measuring IL-2 and IFNγ in culture supernatant. Results: The proliferation ability of cells in vitro was the same (P = 0.782). After inoculation of different tumor cells, all three groups of tumors developed tumors, and the tumors in the inoculated H2 2 / B7-2 group had delayed development. After 18 days of inoculation Tumor began to shrink, but eventually did not disappear completely; tumor inoculation of H2 2 / Wt and H2 2 / neo groups showed progressive growth. The ability of H2 2 / B7-2 to stimulate lymphocyte proliferation and induce CTLs in vitro was significantly stronger than that of control cells (P <0.05). Conclusion: The co-stimulatory molecule B7-2 can enhance the immunogenicity of hepatocarcinoma cells and play an important role in anti-tumor early stage. The treatment of liver cancer with it is effective, but can not mediate complete and long-term anti-tumor effect.