小鼠黑素瘤细胞培养上清对同型小鼠淋巴细胞转铁蛋白受体CD71的抑制作用分析  

Inhibition analysis of the mouse melanoma cell culture supernatant to the same type of mouse lymphocyte transferrin receptor CD71

作　　者：赵红侠[1] 蒋苗苗[1] 孙立新[1] 

机构地区：[1]承德医学院附属医院中心实验室,河北省承德市067000

出　　处：《临床合理用药杂志》2012年第13期7-8,共2页Chinese Journal of Clinical Rational Drug Use

摘　　要：目的通过检测小鼠黑色素瘤细胞(B16F10)培养上清对同型小鼠淋巴细胞活化分子CD71表达的抑制,探讨黑素瘤细胞抑制淋巴细胞活化、介导肿瘤细胞免疫逃逸的机制。方法用B16F10培养上清培养同型小鼠脾淋巴细胞(上清组),经植物血凝素活化,用流式细胞仪检测小鼠脾淋巴细胞转铁蛋白受体CD71表达水平,用RPMI1640完全培养液代替B16F10培养上清作为对照组。结果上清组培养上清培养的淋巴细胞CD71表达率为(55.41±3.70)%低于对照组的(60.92±2.02)%,差异有统计学意义(P<0.05)。结论 B16F10培养上清对淋巴细胞表达CD71具有抑制作用,可抑制淋巴细胞活化,成为免疫逃逸机制之一。Objective Through the detection of mouse melanoma cell（B16F10） culture supernatant of lymphocyte activation molecule CD71 expression in the same type of mice,to explore the melanoma cell inhibit lymphocyte activation,mediate tumor cell immune escape mechanisms.Methods B16F10 culture supernatants of the same type of mouse spleen lymphocytes（experimental group） by phytohemagglutinin activation of the transferrin receptor CD71 expression level,measured by flow cytometry of mouse spleen lymphocytes with RPMI 1640 complete medium instead of B16F10 cultureclear as the control group.Results The expression of CD71 in experimental group[（55.41±3.70）%] was lower than that in control group[（60.92±2.02）%],the difference was statistically significant（P〈0.05）.Conclusion B16F10 culture supernatant inhibited expression of CD71 on lymphocytes,inhibit lymphocyte activation,becoming immune to one of the escape mechanism.

关 键 词：黑色素瘤细胞 淋巴细胞 CD71 

分 类 号：R739.5[医药卫生—肿瘤]