摘要
目的:通过检测肿瘤组织和肿瘤抗原诱导的小鼠脾脏巨噬细胞B7-H4表达、同时检测荷瘤小鼠T细胞BTLA的表达,以进一步探讨这一对新的负免疫调节分子在肿瘤免疫逃逸机制中的作用。方法:应用RT-PCR检测体外培养肿瘤细胞株3LL和Renca、荷瘤后小鼠肿瘤组织B7-H4mRNA以及荷瘤小鼠T细胞BTLA mRNA表达的改变;应用流式细胞术检测荷瘤小鼠脾脏巨噬细胞和肿瘤可溶性抗原诱导的正常小鼠脾脏巨噬细胞B7-H4表面蛋白表达的改变;应用免疫组化技术检测荷瘤后小鼠肿瘤组织B7-H4表面蛋白表达的改变。结果:在体外培养的肿瘤细胞株3LL和Renca上未检测到B7-H4mRNA的表达,小鼠成瘤后肿瘤组织和脾脏巨噬细胞在mRNA水平和蛋白质水平上均高表达B7-H4。另外荷瘤小鼠的T细胞较正常小鼠T细胞BTLA的表达明显增高。在体外肿瘤抗原刺激下,正常小鼠脾脏巨噬细胞B7-H4表达量明显上升;而用正常同样组织来源抗原刺激时,正常小鼠脾脏巨噬细胞B7-H4表达量未见显著改变。结论:B7-H4和BTLA这对协同刺激分子的异常表达可能在肿瘤逃逸免疫应答过程中起调节作用。
Purpose：To further investigate the rule of the novel egative immuno-regulatory molecules in tumor evasion by testing B7-H4 expression on tumor tissues and spleen macophages induced by tumor antigen of mice and BTLA expression on Tcells of the tumor cell lines （3LL and Renca）in citro,tumor tissues and the expression of BTLA mRNA of the tumor bearing mice Tcells;via flow eytometry,we evaluaed the differences in the expression of B7-H4 surface protein of the spleen macrophages from tumor bearing mice and the normal spleen macrophages after stimulation with the tumor antigen,Moreover,via immunohistochemistry,we also evaluated the differences in the expression of B7-H4 surlace protein of tumor tissues.Results：Tumor cell lines （3LL and Renca）did not express the B7-H4 mRNA in ritro.All tumor tissues or spleen macrophages in tumor bearing mice have a high expression of both B7-H4 mRNA and B7-H4protein.Compared with those from normal mice,T cells from tumor bearing micc showed a higher expression of BTLA.Stimulated by tumor antigen in vitro,normal mice spleen marophages B7-H4 expression inereased signifieantly;while no apparent difference was found in the groups stimulated by the corresponding normal tissue antigen.Coclusions：The aberrant expression of the costimulatory molecules,B7-H4 and its receptor BTLA.may have a regulatie effect in tumor evasion immunity.
出处
《中国癌症杂志》
CAS
CSCD
2005年第4期313-316,共4页
China Oncology
基金
复旦大学"筠政学者"基金资助。
