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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1991-8-9
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pubmed:abstractText |
Mouse Sal sarcoma cells are lethal in the autologous A/J (KkDd) host. In order to improve the immune response to the Sal tumor, Sal cells have been transfected with syngeneic MHC-class-II or allogeneic MHC-class-I genes. MHC-class-II transfectants are uniformly rejected by the autologous host and immunization with them protects against subsequent Sal challenge. The improved immunity is probably the result of enhanced generation of tumor-specific Th cells. We hypothesize that class-II tumor cells trigger an improved Th-cell response because they directly present Sal tumor antigens in the context of class-II molecules to Th cells, by-passing professional APC. Studies by others have demonstrated that antigen presentation requires an intracellular signal transmitted by the cytoplasmic domain of the APC class-II molecule. Sal cells expressing class-II antigens with truncated cytoplasmic domains are as malignant as wild-type Sal cells. These experiments therefore support the role of tumor-cell class-II molecules as antigen presentation elements, and demonstrate the requirement for intact class-II molecules for tumor protection. Sal cells have also been transfected with allogeneic MHC-class-I genes. Although Kb-transfected cells are not rejected by A/J mice, Db-transfected Sal cells and Kb- plus Db-transfected cells are rejected. The Db transfectants effectively immunize A/J mice against subsequent Sal challenge. These experiments demonstrate that expression of certain allogeneic MHC-class-I genes can lead to tumor-specific immunity, and that such transfectants can protect against challenges of wild-type tumor cells. Transfection of tumor cells with syngeneic MHC-class-II or allogeneic MHC-class-I genes may therefore be a potential strategy for improving tumor-specific immunity in the autologous host.
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pubmed:grant | |
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:issn |
0898-6924
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
61-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1906055-Animals,
pubmed-meshheading:1906055-Antibodies, Monoclonal,
pubmed-meshheading:1906055-Cell Line,
pubmed-meshheading:1906055-Genes, MHC Class I,
pubmed-meshheading:1906055-Genes, MHC Class II,
pubmed-meshheading:1906055-Graft Rejection,
pubmed-meshheading:1906055-Histocompatibility Antigens Class II,
pubmed-meshheading:1906055-Mice,
pubmed-meshheading:1906055-Mice, Inbred A,
pubmed-meshheading:1906055-Models, Biological,
pubmed-meshheading:1906055-Neoplasm Transplantation,
pubmed-meshheading:1906055-Sarcoma, Experimental,
pubmed-meshheading:1906055-T-Lymphocytes,
pubmed-meshheading:1906055-Transfection
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pubmed:year |
1991
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pubmed:articleTitle |
Tumor-specific immunity can be enhanced by transfection of tumor cells with syngeneic MHC-class-II genes or allogeneic MHC-class-I genes.
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pubmed:affiliation |
Department of Biological Sciences, University of Maryland Baltimore County 21228.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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