肿瘤细胞分泌物抑制树突状细胞的生成和功能  

Suppression of the Development and Function of Dendritic Cells by the Secretion of Tumor Cells

作　　者：李春昭[1] 侯春梅[2] 吴英[2] 张双喜[2] 郭子宽[2] 毛宁[2] 

机构地区：[1]北京军区总医院消化内科,北京100700 [2]军事医学科学院基础医学研究所

出　　处：《中国肿瘤生物治疗杂志》2002年第2期105-109,共5页Chinese Journal of Cancer Biotherapy

摘　　要：目的：探讨肿瘤细胞对人单个核细胞源树突状细胞（dendritic cells,DC）的生成和功能的影响。方法：培养外周血单个核细胞源DC，体系中加入人肝癌细胞系H7402，结肠癌细胞系HCT－8及正常人骨髓基质细胞系HFCL的培养上清液，以正常培养体系为对照。应用流式技术检测DC的细胞表面标志及吞噬功能；通过[^3H]－TdR掺入法检测DC激活同种异体T淋巴细胞活化的能力。结果：H7402和HCT－8细胞培养上清液作为条件培养的DC，低表达CD1a抗原、共刺激分子（CD86）及MHC-Ⅱ类分子，与对照及基质细胞组比较有明显差异。DC成熟也受到抑制。此外，DC对葡聚糖（Dextran）的吞噬功能下降，对同种异常T淋巴细胞激活的能力较低。结论：肿瘤细胞分泌的某些物质可抑制DC的生成及其相关功能，这可能是肿瘤细胞逃避机体免疫监视的机制之一。Objective: To explore the effects of tumor cells on the development and function of the mononuclear cell (MNC) -derived dendritic cells. Methods: The supernatants of cultured cell lines H7402 (human hepatocellular carcinoma) , HCT-8 (human colon carcinoma) and HFCL (human bone marrow stromal cell) were collected and used as the conditional culture medium (CCM) for MNC-derived DC culture. The dendritic cells were characterized by phenotypic a-nalysis. We evaluated the capacity of phagocytizing dextran, and the capacity to stimulate allogeneic T cells of MNC-derived DC. Results:Phenotypic analysis showed that dendritic cells cultured in the presence of supernatants of tumor cells expressed lower levels of GDI a, MHC Ⅱ molecules (HLA-DR) and costimulatory molecules (CD86) , all of which were significantly lower than those in control and HFCL groups (the negative control group). Also, they displayed a much lower capacity of phagocytizing dextran as shown by the FITC-dextran assay. Moreover, they were less efficient of inducing allogeneic T-cell proliferation in a mixed lymphocyte reaction. Conclusion: These data show that tumor cells negatively regulate the production and function of DC, which might be one of the underlying mechanisms that play a role in the immune escape of tumor cells.

关 键 词：单个核细胞源树突状细胞 肿瘤细胞 免疫逃逸 DC 

分 类 号：R730.3[医药卫生—肿瘤] R392.12[医药卫生—临床医学]