PHA诱导B16F10黑素瘤细胞上清培养的小鼠淋巴细胞中IL-2和FasL的变化

The Changes of IL-2,FasL Secretion in PHA Stimulated Mouse Lymphocytes Cultured with Supernatant of B16F10 Cell Culture

目的探讨B16F10黑素瘤细胞培养上清对PHA刺激同基因小鼠脾淋巴细胞产生IL-2和表达FasL的影响。方法将C57BL/6小鼠脾淋巴细胞培养于B16F10黑素瘤细胞培养上清或正常培养基中,经PHA激活72h后,用免疫细胞组化法及Western blot法检测小鼠脾淋巴细胞IL-2的水平;用免疫荧光染色及Western blot法检测小鼠淋巴细胞FasL的表达。结果 B16F10细胞培养上清组同基因小鼠脾淋巴细胞产生IL-2及表达FasL较正常培养基对照组均显著下降。结论 B16F10细胞培养上清可抑制PHA刺激小鼠脾淋巴细胞产生IL-2和表达FasL,提示B16F10黑素瘤细胞抑制淋巴细胞产生IL-2及表达FasL可能是其实现肿瘤细胞免疫逃逸的机制之一。

Objective To observe the effect of culture supernatant of BI6F10 cells on IL-2, FasL expressed by the PHA stimulated sygeneous mouse spleen lymphocytes. Methods The mouse spleen lymphocytes were induced by PHA and cuhured in the supernatant of B16F10 cell culture or the normal control medium for 72h, then the immunocytochemistry and the western blot was used to display the IL-2 in the lymphocytes; the immunofluorescent test and the western blot was used to display the FasL in the lymphocytes. Results As compared with the normal medium control group, IL-2, FasL produced by sygeneous mouse spleen lymphocyte treated by supernatant of BI 6F10 cell culture was decreased （ P 〈 0. 005 ）. Conclusion [L-2, FasL expressed by mouse spleen lymphocyte induced by PHA can be suppressed by treatment with the supernatant of B16F10 cell culture, implying that the suppression on IL-2, FasL produced by immune ceils may contribute to immune escape of BI6FIO cell.