B7-H1分子在肿瘤微环境中的特异表达及对调节性T细胞的诱导促进作用

目的通过分析人结直肠癌细胞表达B7-H1分子与肿瘤微环境中浸润的调节性T细胞的关系,探讨肿瘤性B7-H1信号参与肿瘤免疫逃逸的机制。方法采用免疫组化分析肠癌组织中B7-H1分子的表达及调节性T细胞的浸润情况,采用细胞培养和流式细胞术分析肿瘤性B7-H1信号对调节性T细胞分化的作用。结果 B7-H1异常高表达在肠癌组织中,正常组织不表达;肿瘤组织中B7-H1表达水平与调节性T细胞浸润数量成正相关（P〈0.01）,在TGFβ-的共同作用下,M435-B7-H1细胞可以显著促进Tregs的诱导。结论 B7-H1在肿瘤组织异常表达可通过诱导肿瘤微环境中调节性T细胞的分化参与肿瘤免疫逃逸。

Abnormal Expression of B7-H1 in the Tumor Microenvironment and the Promotion of the Regulatory T Cell Expansion

Objective To explore the mechanism of B7-H1 signal involved in tumor immune escape by the analysis of the B7-H1 expression in colorectal carcinoma and the regulatory T cell infiltration.Methods IHC staining was used to detect the B7-H1 expression and regulatory T cell infiltration,cell culture and Flow cytometry analysis were used to analyze the effect of B7-H1 signal to induction of regulatory T cell.Results B7-H1 was found abnormally expressed in tumor tissues,and the regulatory T cell infiltration was also confirmed.The expression level of B7-H1 was positively correlated to regulatory T cell density,and the tumor-associated B7-H1 could induce the generation of regulatory T cell in vitro.Conclusion The over-expression of B7-H1 is involved immune escape via the induction of regulatory T cell in tumor microenvironment.