The Therapeutic Effect of Cytokine-Induced Killer Cells on Pancreatic Cancer Enhanced by Dendritic Cells Pulsed with K-Ras Mutant Peptide

摘要

Objective . This study is to investigate the role of the CIKs cocultured with K-ras-DCs in killing of pancreatic cancer cell lines, PANC-1 (K-ras~(+)) and SW1990 (K-ras~(?)). Methods . CIKs induced by IFN- γ , IL-2, and anti-CD3 monoantibody, K-ras-DCCIKs obtained by cocultivation of k-ras-DCs and CIKs. Surface markers examined by FACS. IFN- γ IL-12 ,CCL19 and CCL22 detected by ELISA. Proliferation of various CIKs tested via 3H-TdR. Killing activities of k-ras-DCCIKs and CTLs examined with 125IUdR. Results . CD3~(+)CD56~(+)and CD3~(+)CD8~(+)were highly expressed by K-ras-DCCIKs. In its supernatant, IFN- γ , IL-12, CCL19 and CCL22 were significantly higher than those in DCCIK and CIK. The killing rate of K-ras-DCCIK was greater than those of CIK and CTL. CTL induced by K-ras-DCs only inhibited the PANC-1 cells. Conclusions . The k-ras-DC can enhance CIK's proliferation and increase the killing effect on pancreatic cancer cell. The CTLs induced by K-ras-DC can only inhibit PANC-1 cells. In this study, K-ras-DCCIKs also show the specific inhibition to PANC-1 cells, their tumor suppression is almost same with the CTLs, their total tumor inhibitory efficiency is higher than that of the CTLs.