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

Abstract EN

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.