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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
17
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pubmed:dateCreated |
1988-9-26
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pubmed:abstractText |
As an initial approach to experiments directed toward effective adoptive immunotherapy for cancer using lymphokine genes, we transferred retrovirally a complementary DNA encoding mouse gamma-interferon (IFN-gamma) into a specific cytotoxic T-lymphocyte clone, designated E-4, against 203 glioma cells (a 20-methylcholanthrene-induced mouse glioma line) and confirmed the efficacy of IFN-gamma production from the exogenous gene on augmentation of tumor targeting. Of five, two gene-transferred subclones constitutively produced 8 to 10 times the amount of IFN-gamma as compared with the parental E-4. Correspondingly, these two subclones exhibited 2 to 3 times higher killing activity against 203 glioma than the parental cells; the enhancement of the killing activities was abrogated by an adequate addition of anti-IFN-gamma antibody. No alteration was seen after the gene transfer in cell surface phenotypes, Thy-1+, Lyt-1-, Lyt-2+,3+, and asialo-GM1-. The surface expression of a major histocompatibility complex Class I antigen, H-2Kb, was not altered remarkably, but the Class II antigen, I-Ab, was partially and slightly enhanced on the two IFN-gamma-producing sublines mentioned above on fluorescence-activated cell sorter analysis. Since it is considered that in the vicinity of the constitutively IFN-gamma producing cytotoxic T-lymphocyte cells tumor cells are exposed to a high concentration of IFN-gamma, the cells may be stimulated to induce or enhance the expression of surface antigens including major histocompatibility complex antigens as well as tumor-associated antigens relevant to immune recognition. The 203 glioma cells pretreated with IFN-gamma were more efficiently killed by both the parental E-4 and the gene-transferred sublines. Taken together, the results suggested that the augmented specific tumor-killing activity of our gene-transferred cytotoxic T-lymphocytes was ascribed to the constitutive production of IFN-gamma derived from the exogenous gene.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4730-5
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:3136912-Animals,
pubmed-meshheading:3136912-Antigens, Surface,
pubmed-meshheading:3136912-Cell Line,
pubmed-meshheading:3136912-DNA,
pubmed-meshheading:3136912-Glioma,
pubmed-meshheading:3136912-Immunotherapy,
pubmed-meshheading:3136912-Interferon-gamma,
pubmed-meshheading:3136912-Male,
pubmed-meshheading:3136912-Mice,
pubmed-meshheading:3136912-Mice, Inbred C57BL,
pubmed-meshheading:3136912-Retroviridae,
pubmed-meshheading:3136912-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:3136912-Transfection
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pubmed:year |
1988
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pubmed:articleTitle |
Augmentation of tumor targeting in a line of glioma-specific mouse cytotoxic T-lymphocytes by retroviral expression of mouse gamma-interferon complementary DNA.
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pubmed:affiliation |
Department of Neurosurgery, Medical School, Kyoto University, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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