摘要目的 检测B7-H1和IL-10在胰腺癌组织中的表达情况,并分析两者表达水平的相关性,以探讨肿瘤局部IL-10的异常增高和B7-H1表达的关系.方法 应用RT-PCR、Western blot和免疫组织化学法检测35例胰腺癌组织、相应癌旁组织和5例正常胰腺组织中B7-H1及IL-10的表达情况,并分析其相关性.结果 在胰腺癌、癌旁和正常胰腺组织中,B7-H1和IL-10在mRNA及蛋白水平的表达呈现出明显由高至低的趋势,且两两之间比较均具有明显差异(P<0.05),免疫组织化学结果也同样证实了胰腺癌中高表达B7-H1和IL-10,阳性率分别为60.5%±12.7%和65.3%±16.2%,而正常组织中未检测到表达.同时,相关性分析中显示肿瘤组织B7-H1高表达与IL-10水平呈明显正相关,分别表现在mRNA表达水平(P=0.008,r=0.841)和蛋白表达水平(P=0.007,r=0.838).结论 胰腺癌细胞上调表达B7-H1可能是肿瘤局部高浓度IL-10形成的原因之一,由此导致的抗肿瘤免疫能力降低可使肿瘤细胞逃避免疫系统的杀伤作用.
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abstractsObjective To investigate the role of B7-H1 expression in IL-10 production,the B7-H1 and IL-10 expression levels in pancreatic carcinoma tissues and to analyze the correlation between B7-H1 expression and IL-10 level.Methods The mRNA and protein levels expressions of BT-H1 and IL-10 in 35 cases of pancreatic cancer and corresponding paracaminoma tissues and 5 cases of normal pancreas tissues were detected by RT-PCR,Western blot and immunohistochemistry respectively.Results The findings for the first time provided the evidences that there was a clear trend for B7-H1 and IL-10 expressions to be most highly expressed in carcinoma tissue,intermediately expressed in paracarninoma tissue,and expressed at the lowest level in normal pancreatic tissue at mRNA and protein levels.Moreover,there were statistically significant differences in B7-H1 and IL-10 expression between pancreatic carcinoma tissues,corresponding paracarcinoma tissues and normal pancreatic tissues at mRNA and protein levels (P<0.05).Furthermore,the immunohistochemistry indicated that there were high expression levels of B7-H1 (60.5%±12.7% ) and IL-10 (65.3%±16.2%) in pancreatic carcinoma tissues while there were no significant expressions in normal pancreatic tissues.Meanwhile,correlation analysis revealed that B7-H1 expression was significant associated with IL-10 level in tumor tissues at mRNA (P=0.008,r=0.841) and protein levels (P=0.007,r=0.838).Conclusions Over-expression of B7-H1 may be responsible for the increasing IL-10 production in pancreatic cancer,which caused reduced immune response to tumor cells and contributed to pancreatic carcinoma escape from immune attack.
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