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。应用流式细胞技术检测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，对同种异体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 conditionalculture medium (CCM) for MNC-derived DC culture. The dendritic cells were characterized by phenotypic analysis. 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 CD1a, 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.