Lee Wei-Chen, Chiang Yang-Jen, Wang Hui-Chuan, Wang Min-Ru, Lia Shin-Ru, Chen Miin-Fu
Laboratory of Immunology, Department of General Surgery, Chang-Gung Memorial Hospital, Taipei, Taiwan.
J Clin Immunol. 2004 Mar;24(2):145-54. doi: 10.1023/B:JOCI.0000019779.56180.a2.
Immunosuppression in tumor-bearing hosts may be a major obstacle in eradicating tumors. This study investigated whether hepatocellular carcinoma suppressed the functions of dendritic cells to escape tumor surveillance. Dendritic cells (DC), propagated from C57BL/10J mice, were cocultured with or without murine hepatoma Hepa1-6 cells to examine the influence of hepatocellular carcinoma on dendritic cells. The results revealed that dendritic cells cocultured with hepatoma cells expressed low levels of costimulatory molecules, and the stimulatory capacity was decreased. The antigen-specific cytotoxic effects of T cells activated by the DC cocultured with hepatoma cells were also decreased. In ex vivo studies, the maturation and function of dendritic cells propagated from tumor-bearing mice were suppressed. The suppressive effect of Hepa1-6 cells on dendritic cells could be partially reversed by neutralizing IL-10. In conclusion, the maturation and stimulatory function of DC are suppressed by hepatocellular carcinoma. IL-10 release may be one of the mechanisms employed by hepatocellular carcinoma to suppress dendritic cells.
荷瘤宿主中的免疫抑制可能是根除肿瘤的主要障碍。本研究调查了肝细胞癌是否通过抑制树突状细胞的功能来逃避肿瘤监视。从C57BL/10J小鼠中培养的树突状细胞（DC）与鼠肝癌Hepa1-6细胞共培养或不共培养，以研究肝细胞癌对树突状细胞的影响。结果显示，与肝癌细胞共培养的树突状细胞共刺激分子表达水平较低，刺激能力下降。由与肝癌细胞共培养的DC激活的T细胞的抗原特异性细胞毒性作用也降低。在体外研究中，荷瘤小鼠来源的树突状细胞的成熟和功能受到抑制。中和IL-10可部分逆转Hepa1-6细胞对树突状细胞的抑制作用。总之，肝细胞癌抑制DC的成熟和刺激功能。IL-10释放可能是肝细胞癌抑制树突状细胞的机制之一。
