中文摘要：

我们学习了的目的特定的细胞毒素的 T 淋巴细胞(CTL ) 的角色由与在杀死不同胰腺的癌症房间的变异的肽和整个肿瘤抗原在 vitro 并且在 vitro 衬里的 K 地岬(12-Val ) 介绍 cationic nanoparticles 的树枝状的房间(DC ) 激活。方法外部血 DC 被 rhGM-CSF 和 IL-4 导致并且有教养。DC 被一根胰腺的癌症房间线(PANC-1 ) 的整个抗原分别地与 K 地岬变异的肽(K-ras+peptide-CNP ) 与 K 地岬异种， K 地岬变异的肽(K-ras+peptide ) 和 cationic nanoparticles 的表示敏化。房间表面标记被流动 cytometry 测量。淋巴细胞增长被 3H-TdR 测试检测，并且 ELISA 被执行检测 IFN- 分泌物。125I-UdR 被用来测量 CTL 的杀死的效果。我们也在与 PANC-1 (K-ras+) 和 SW1990 准备的一个忍受肿瘤的裸体老鼠模特儿在 vivo 评估了 CTL 的 antitumor 活动(K 地岬 ?) 房间线。与 K-ras+peptide 相比结果，低集中 K-ras+peptide-CNP 能被 DC 有效地介绍(P < 0.05 ) 。DC 导致的 CTL 与肿瘤抗原让重要更大的杀死完成的全部搏动了(P < 0.05 ) 在 PANC-1 和 SW1990 上胰腺的癌症房间与 K-ras+peptide 和 K-ras+peptide-CNP-induced CTL 相比。DC 导致的 CTL 与 K-ras+peptide 搏动了， K-ras+peptide-CNP 有特定的杀死效果(P < 0.05 ) 为 PANC-1 和没有效果(P > 0.05 ) 在 SW1990 房间线上(P > 0.05 ) 。有 K 地岬(12-Val ) 的结论 Cationic nanoparticles 变异的肽能被 DC 有效地在一短时间在低集中介绍。K-ras+peptide-CNP 导致的 CTL 为胰腺的癌症房间举办了特定的杀死的活动与 K 地岬(12-Val ) 异种排队并且能显著地禁止肿瘤生长并且增加忍受肿瘤的裸体老鼠的幸存时间。

英文摘要：

Objective： We studied the role of specific cytotoxic T lymphocytes （CTLs） activated by dendritic cells （DCs） presenting cationic nanoparticles with the K-ras （12-Val） mutant peptide and whole tumor antigen in the killing of different pancreatic cancer cell lines in vitro and in vitro. Methods： Peripheral blood DCs were induced by rhGM-CSF and IL-4 and cultured. DCs were sensitized by whole antigen of a pancreatic cancer cell line （PANC-1） with expression of K-ras mutant, K-ras mutant peptide （K-ras＋peptide） and cationic nanoparticles with K-ras mutant peptide （K-ras＋peptide-CNP）, respectively. Cell surface markers were measured by flow cytometry. Lymphocyte proliferation was detected by the 3H-TdR test, and ELISAwas performed to detect IFN-y secretion. 125I-UdR was used to measure the killing effect of CTLs. We also evaluated the antitumor activity of CTLs in vivo in a tumor-bearing nude mouse model prepared with the PANC-1 （K-ras＋） and SW1990 （K-ras-） cell lines. Results： Compared with K-ras＋peptide, low concentration K-ras＋pepUde-CNP can be effectively presented by DCs （P 〈 0.05）. CTLs induced by DCs pulsed with whole tumor antigen had significant greater killing effect （P 〈 0.05） on PANC-1 and SW1990 pancreatic cancer cells compared with K-ras＋peptide and K-ras＋peptide-CNP-induced CTLs. CTLs induced by DCs pulsed with K-ras＋peptide and K-ras＋peptide-CNP had a specific killing effect （P 〈 0.05） for PANC-1 and no effect （P 〉 0.05） on SW1990 cell lines （P 〉 0.05）. Conclusion： Cationic nanoparticles with K-ras （12-Val） mutant peptide can be effectively presented by DCs at a low concentration in a short time. CTLs induced by K-ras＋peptide-CNP had specific killing activity for the pancreatic cancer cell line with the K-ras （12-Val） mutant and could significantly inhibit tumor growth and increase the survival time of tumor-bearing nude mice.