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目的 :研究HLA I分子表达与B7 1分子的共刺激作用的相互关系 ,以探讨在肿瘤细胞所诱发的免疫排斥反应中共刺激分子对抗原递呈机制的影响。方法 :通过流式细胞仪 (FCM)检测转染共刺激分子B7 1编码基因前后其表面HLA I分子的表达情况。利用单克隆抗体阻断细胞表面HLA I分子 ,以外周血混合淋巴细胞对阻断前后的细胞行杀伤实验。结果 :表达B7 1的肝癌细胞其表面HLA I分子表达明显增高 (P <0 0 1) ,而γ INF刺激对细胞表面HLA I分子的表达情况并无影响(P >0 0 5 )。T淋巴细胞对转染后细胞的杀伤作用远远大于未转染组 (P <0 0 1) ,当表面HLA I分子被阻断后 ,T淋巴细胞的杀伤效应几乎降至零点。结论 :转染B7 1后肝癌细胞高表达HLA I分子 ,增强抗原提呈作用的同时又表达第二信号—共刺激分子B7 1,从而可诱发更强的免疫排斥反应。
OBJECTIVE: To study the relationship between the expression of HLA I molecules and the co-stimulatory effect of B7 1 molecule in order to explore the effect of co-stimulatory molecules on antigen presenting mechanism in tumor rejection induced by tumor cells. Methods: The expression of HLA I on the surface of B7 1 gene was detected by flow cytometry (FCM). Monoclonal antibodies were used to block HLA-I molecules on the cell surface and peripheral blood mixed lymphocytes were used to kill the cells before and after the blocking. Results: The expression of HLA I on the surface of B7 1 cells was significantly increased (P <0.01), but not on the expression of HLA I molecules on the surface of B7 1 cells (P> 0.05). The cytotoxicity of T lymphocytes to transfected cells was much greater than that of untransfected cells (P <0.01). When HLA I molecules were blocked, the killing effect of T lymphocytes almost dropped to zero. CONCLUSION: H7 cells transfected with B7 1 highly express HLA I molecules, enhance the antigen presentation and express the second signal-costimulatory molecule B7 1, which can induce stronger immune rejection.