Abstract
hTERTC27, a 27-kDa hTERT C-terminal polypeptide has been demonstrated to cause hTERT-positive HeLa cell apoptosis and inhibits the growth of mouse melanoma. hTERTC27 has been associated with telomere dysfunction, regulation of gene-regulated apoptosis, the cell cycle and activation of natural killer (NK) cells, but its mechanism of action is not fully understood. Here, we report that dendritic cells (DCs) transduced with hTERTC27 can increase T-cell proliferation, and augment the concentration of interleukin-2 (IL-2) and interferon-γ (IFN-γ) in the supernatants of T cells. It can also induce antigen-specific cytotoxic T lymphocytes (CTL) against glioma cells in vitro. Moreover, hTERTC27 gene-transduced DCs exhibit a very potent cytotoxicity to glioma cells in vivo. It could prolong the survival time and inhibit the growth of glioma-bearing mice. These data suggest that hTERTC27 gene-transduced DCs can efficiently enhance immunity against gliomas in vitro and in vivo.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptive Immunity
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Adenoviridae / enzymology*
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Adenoviridae / genetics
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Animals
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Brain Neoplasms / enzymology
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Brain Neoplasms / genetics
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Brain Neoplasms / immunology
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Brain Neoplasms / pathology
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Brain Neoplasms / therapy*
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Cell Line, Tumor
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Cell Proliferation
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Coculture Techniques
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Dendritic Cells / enzymology
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Dendritic Cells / immunology
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Dendritic Cells / transplantation*
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Female
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Genetic Therapy / methods*
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Genetic Vectors*
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Glioma / enzymology
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Glioma / genetics
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Glioma / immunology
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Glioma / pathology
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Glioma / therapy*
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Humans
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Interferon-gamma / metabolism
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Interleukin-2 / metabolism
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Mice
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Mice, Inbred C57BL
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Peptide Fragments / genetics
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Peptide Fragments / metabolism*
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Phenotype
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T-Lymphocytes / immunology
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T-Lymphocytes, Cytotoxic / immunology
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Telomerase / genetics
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Telomerase / metabolism*
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Time Factors
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Transduction, Genetic*
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Tumor Burden
Substances
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Interleukin-2
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Peptide Fragments
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Interferon-gamma
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TERT protein, human
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Telomerase