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4-1BB Protects Dendritic Cells from Prostate Cancer-Induced Apoptosis

机译:4-1BB保护树突状细胞免受前列腺癌诱导的细胞凋亡

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It has been shown that human prostate cancer (PCa) cells induced apoptotic death of the most potent antigen-presenting cells, dendritic cells (DCs), which are responsible for the induction of specific antitumor immune responses. Here, we investigated the function of 4-1BB on protecting DCs from prostate cancer-induced apoptosis with an agonistic mAb to 4-1BB. RM-1 cells and DCs were co-incubated for 48?h and DC apoptosis was assessed by Annexin Vassay. TNF-α and IL-12 production were assessed by enzyme-linked immunosorbent assay (ELISA) and Bcl-2 and Bcl-xL on DCs were analyzed by Western blot. We have shown that co-incubation of RM-1 cells with DCs is accompanied by an increased level of DCs apoptosis. Triggering 4-1BB on DCs resulted in increased resistance of DCs to RM-1 cells-induced apoptosis, which was owing to the up-regulated expression of Bcl-2 and Bcl-xL, and increased secretion of TNF-αand IL-12. These results demonstrate that triggering 4-1BB on DCs could increased resistance of DCs to PCa-induced apoptosis.
机译:已经显示,人前列腺癌(PCa)细胞诱导最有效的抗原呈递细胞树突细胞(DC)的凋亡死亡,其负责诱导特异性抗肿瘤免疫应答。在这里,我们研究了4-1BB在保护DC免受前列腺癌诱导的与4-1BB竞争的mAb凋亡中的功能。将RM-1细胞和DC共孵育48小时,并通过Annexin Vassay评估DC凋亡。通过酶联免疫吸附试验(ELISA)评估TNF-α和IL-12的产生,并通过蛋白质印迹分析DC上的Bcl-2和Bcl-xL。我们已经显示RM-1细胞与DC共同孵育伴随着DC凋亡水平的提高。触发DC上的4-1BB导致DC对RM-1细胞诱导的凋亡的抵抗力增加,这是由于Bcl-2和Bcl-xL的表达上调,以及TNF-α和IL-12的分泌增加所致。这些结果表明,触发DC上的4-1BB可以增加DC对PCa诱导的细胞凋亡的抵抗力。

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