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[The killing effect of cytotoxic T lymphocytes on esophageal adenocarcinoma cells mediated by gp96-peptide complexes].

Authors :
Ma LP
Pan XY
Li N
Liu YJ
Chen XX
Source :
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences [Beijing Da Xue Xue Bao Yi Xue Ban] 2004 Oct; Vol. 36 (5), pp. 525-8.
Publication Year :
2004

Abstract

Objective: To study the immunotherapeutic effect on the esophageal adenocarcinoma mediated by gp96-peptide complexes isolated from the same kind of tumor.<br />Methods: gp96-peptide complexes were purified from nude mice tumors burdened by subcutaneous injection of human esophageal adenocarcinoma cell line SEG-1. gp96-peptide complexes were carried by the dendritic cells(DC) induced from human peripheral blood mononuclear cells to prepare gp96-DC vaccine. The proliferation of lymphocytes was tested with trypan-blue stain. The quantity of interferon-gamma(IFN-gamma) released from cytotoxic T lymphocytes (CTL) was detected with ELISA method. The killing effect of CTL on target cell SEG-1 was measured with MTT.<br />Results: We obtained 120 microg gp96 from 55 g tumor tissue. DC, gp96, and gp96-DC all could elicit the proliferation of lymphocytes and make them becoming into CTL which released IFN-gamma and showed different degrees of killing effect on target cell SEG-1. gp96-DC has the strongest eliciting effect among them. At the ratio of E(effect) to T(target) as 40:1,the killing rate was 68%. No significant difference between the effects of CTL induced by DC alone and of lymphocytes without specific antigen on SEG-1 and K562 cells.<br />Conclusion: The gp96-peptide complexes from tumors can improve the effect of eliciting lymphocyte proliferation of DC and make the lymphocyte becoming into CTL more effectively. These CTLs show prominent killing effect on the target tumor cells.

Details

Language :
Chinese
ISSN :
1671-167X
Volume :
36
Issue :
5
Database :
MEDLINE
Journal :
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
Publication Type :
Academic Journal
Accession number :
15489936