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目的研究4-1BB信号对肿瘤上清诱导的小鼠骨髓来源树突状细胞(DCs)凋亡的拮抗作用及其机制。方法IL-4和GM-CSF诱导C57BL/6小鼠骨髓细胞,得到未成熟DCs,磁珠纯化。以抗4-1BB激发型抗体2A或CD40激发型抗体1c10刺激DCs,在不同条件下检测DCs的凋亡情况。以抗体标记NFκ-Bp65亚基,激光共聚焦显微镜检测抗4-1BB激发型抗体2A处理后DCs内NFκ-Bp65亚基向核内的转位情况。结果DCs上4-1BB信号的激发能拮抗由B-16肿瘤上清诱导的DCs凋亡,效果低于CD40信号,并能引起NFκ-Bp65亚基向核区转位。结论4-1BB信号的激发提高了DCs抵抗肿瘤上清诱导凋亡的能力,此作用通过包含NFκ-B通路的相关胞内信号传导途径实现。
Objective To investigate the antagonism of 4-1BB signal on the apoptosis of mouse bone marrow-derived dendritic cells (DCs) induced by tumor supernatant and its mechanism. Methods The bone marrow cells of C57BL / 6 mice were induced by IL-4 and GM-CSF, and immature DCs were obtained and purified by magnetic beads. DCs were stimulated with anti-4-1BB-stimulated antibody 2A or CD40-stimulated antibody 1c10, and the apoptosis of DCs was detected under different conditions. The NFκBp65 subunit was labeled with antibody, and the translocation of NFκBp65 subunit to nucleus in DCs treated with anti-4-1BB stimulated antibody 2A was detected by laser confocal microscopy. Results The stimulation of 4-1BB signal on DCs could antagonize the apoptosis of DCs induced by B-16 tumor supernatant, and the effect was less than that of CD40 signal, and led to the translocation of NFκBp65 subunit to nucleus. Conclusions The stimulation of 4-1BB signal enhances the ability of DCs to resist the apoptosis induced by tumor supernatants, and this effect is achieved through the relevant intracellular signaling pathways that include the NFκB pathway.