乳腺癌细胞表面MHCⅡ类抗原和共刺激分子表达的研究

目的研究乳腺癌细胞表面MHCⅡ类抗原与共刺激分子CD40、CD80(B7-1)和CD86(B7-2)的表达.方法采用流式细胞技术检测5株乳腺癌细胞MCF-7、SK-BR-3、T47D、MDA-MB-435s和ZR-75 -30表面MHCⅡ类抗原与共刺激分子CD40、CD80(B7-1)和CD86(B7-2)的表达,并与正常乳腺细胞HBL-100作比较. 结果 5株乳腺癌细胞MHCⅡ类分子表达均与正常乳腺细胞HBL-100差异有显著性(P<0.05), MCF-7细胞表达水平最低,约为HBL-100的1/5.MDA-MB-435s与ZR-75-30细胞表达水平为HBL-100的2倍,MDA-MB-435s荧光强度也比HBL-100及其他乳腺癌细胞高,但MDA-MB -435s细胞表面CD40分子表达水平最低,约为MCF-7与HBL-100 CD40分子表达水平的10%. MDA-MB-435s细胞的CD80和CD86分子表达水平与HBL-100相当(P>0.05),另4株乳腺癌细胞的CD80和CD86分子表达均比HBL-100低(P<0.05). 结论乳腺癌细胞表面MHCⅡ与共刺激分子表达异常,不同细胞表面分子的表达有所差异.乳腺癌细胞可通过这些分子表达异常而发生免疫逃逸.

Major histocompatibility complex class II antigen and costimulatory molecule expression on the surface of breast cancer cells

OBJECTIVE: To study the major histocompatibility complex class II (MHC II) antigen and costimulatory molecules expression on the surface of breast cancer cells. METHODS: MHC II antigen and costimulatory molecule expression on five breast cancer cell lines including MCF-7, SK-BR-3, T47D, MDA-MB-435 and ZR-75-30 were detected through flow cytometery analysis, with their expression level compared with that of normal mammary cell line HBL-100. RESULTS: The MHC II expression level of the five breast cancer cell lines were significantly different from that of HBL-100 (P < 0.05). MHC II antigen expression of MCF-7 cells which was about 20 percent of HBL-100 was the lowest. MDA-MB-435 and ZR-75-30 cell expression levels were twice as much as that of HBL-100, with the fluorescence intensity of MDA-MB-435 the highest of all cells. CD40 molecule expression on the surface of MDA-MB-435 cells was the lowest, which was nearly ten percent of that of MCF-7 and HBL-100 cells. CD80 and CD86 molecule expression showed no difference in MDA-MB-435 or HBL-100 cell (P > 0.05), and those of the other four breast cancer cells were lower than that of HBL-100 (P < 0.05). CONCLUSION: MHC II antigen and costimulatory molecule expression on the surface of breast cancer cells is abnormal, with different molecule expression in different cells. Breast cancer cells can escape immune surveillance through abnormal molecule expression.