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Induction of anti‐tumour immunity by dendritic cells transduced with hTERT recombinant adenovirus in mice
Author(s) -
Chen Ling,
Tang XuDong,
Yu SongTao,
Ai ZhiHua,
Fang DianChun,
Cai YongGuo,
Luo YuanHui,
Liang GuangPing,
Yang ShiMing
Publication year - 2009
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2493
Subject(s) - telomerase reverse transcriptase , cytotoxic t cell , ctl* , biology , dendritic cell , telomerase , transfection , antigen , cancer research , viral vector , virology , immunology , recombinant dna , cell culture , in vitro , cd8 , gene , biochemistry , genetics
Dendritic cells (DCs) transfected with recombinant, replication‐defective adenovirus (Ad) vectors encoding the human telomerase reverse transcriptase (hTERT) are potent inducers of cytotoxic T lymphocytes (CTLs) and anti‐tumour immunity. However, previous studies have mostly been in vitro. In this study, we sought to determine whether DCs transfected with hTERT (DC/Ad‐hTERT) could elicit a potent anti‐tumour immunogenic response in vivo . We found that murine DCs transfected with recombinant adenovirus encoding the hTERT gene (DC/Ad‐hTERT) induced hTERT‐specific CTLs in vivo effectively, compared with Ad‐LacZ‐transduced DC (DC/Ad‐LacZ) controls. These hTERT‐specific CTLs lysed various tumour cell lines in an hTERT‐specific and MHC‐I molecule‐restricted fashion. We also found that DC/Ad‐hTERT could increase antigen‐specific T‐cell proliferation and augment the number of IFN‐γ secreting T‐cells in mice. These data suggest that the DC/Ad‐hTERT vaccine may induce anti‐tumour immunity against tumour cells expressing hTERT in an MHC‐I molecule‐restricted fashion in vivo through the augmentation of the hTERT‐specific CTL response. The DC/Ad‐hTERT vaccine may thus be used as an efficient DC‐based tumour vaccine in clinical applications. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.