摘要
目的:探讨卡介苗(BCG)能否增强抗肿瘤疫苗HSP-MUC1的特异性抑瘤作用,从而将BCG开发为肿瘤疫苗的新型佐剂。方法:动物水平上,BCG和HSP-MUC1共免疫小鼠,观察BCG能否增强HSP-MUC1所激发的特异性抑瘤作用。细胞水平上对BCG发挥佐剂作用的机制进行探讨,将BCG和HSP-MUC1共刺激树突状细胞(DC),观察BCG能否协同HSP-MUC1刺激DC表面的CD86分子表达的上调;并对DC培养上清中IL-6、TNF-α的水平进行测定。结果:BCG+HSP-MUC1组小鼠的肿瘤重量显著地低于HSP-MUC1组(P<0.05)。细胞学试验显示,BCG能够显著增强HSP-MUC1对DC的激活作用,使DC表面的CD86分子显著上调。BCG+HSP-MUC1组的DC培养上清中细胞因子IL-6、TNF-α的水平显著地高于HSP-MUC1组(P<0.05)。结论:BCG能够显著地增强HSP-MUC1的抗肿瘤活性,具有肿瘤疫苗佐剂的良好功效。
Objective：To explore the effects of BCG on the tumor suppression elicited by HSP-MUC1 and develop an effective adjuvant of HSP-MUC1. Methods：In animal experiments, BCG was injected into the mice together with HSP-MUC1 to test if BCG can strengthen the tumor suppression elicited by HSP-MUC1 ; in cellular level, the expression enhancement of CD86 molecules on the surface of dendritic cells by BCG were studied. Results：The tumor weight in mice from BCG ＋ HSP-MUC1 group was significantly less than that from HSP-MUC1 group. The expression of CD86 molecules on the surface of dendritic cells was enhanced by BCG. Conclu- sion：BCG can be used as adjuvant of HSP-MUC1 and enhance the tumor suppression of HSP-MUC1.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2007年第6期526-530,共5页
Chinese Journal of Immunology
基金
国家高科技"863"计划(2002AA214141)资助
