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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
1994-3-21
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pubmed:abstractText |
The co-existence of tumor specific immunity with a progressing tumor is observed in a variety of experimental systems and remains one of the major paradoxes of tumor immunology. We now report that a human melanoma cell line (SMC) expressing MHC class II was able to induce clonal anergy in a specific, MHC-restricted CD4+ T cell clone (STC3). Clonal anergy is a mechanism of T lymphocyte tolerance induced by antigen receptor stimulation in the absence of co-stimulation. We observed that a CD4+ T cell clone and an autologous melanoma cell line form conjugates with each other that leads to an increase of [Ca++]i in the T cell clone; however, this interaction failed to induce IL-2 production or proliferation of the T cell clone. Furthermore, this interaction rendered this T cell clone unresponsive to subsequent stimulation. All these effects were MHC class II restricted. Therefore, the human melanoma cell line SMC was capable of delivering antigen-specific signals to the T cell clone, but did not deliver the co-stimulatory signals, e.g. a B7/CD28 interaction, necessary for full T cell activation. Transfection of the melanoma cells with an expression vector containing a B7 cDNA that resulted in subsequent expression of B7 on its cell surface rendered it into a fully competent antigen presenting cell, which is able to induce a nuclear factor binding to the IL-2 promoter in the specific T cell clone resulting in enhanced IL-2 transcription, synthesis, and T cell proliferation. These findings suggest that manipulation of co-stimulation may offer new strategies for future tumor immunotherapy.
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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 |
Dec
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pubmed:issn |
0953-8178
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1501-8
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:7906140-Base Sequence,
pubmed-meshheading:7906140-Blotting, Northern,
pubmed-meshheading:7906140-CD4-Positive T-Lymphocytes,
pubmed-meshheading:7906140-Calcium,
pubmed-meshheading:7906140-Cell Line,
pubmed-meshheading:7906140-Clonal Anergy,
pubmed-meshheading:7906140-HLA-DR Antigens,
pubmed-meshheading:7906140-Humans,
pubmed-meshheading:7906140-Immunologic Surveillance,
pubmed-meshheading:7906140-Interleukin-2,
pubmed-meshheading:7906140-Lymphocytes, Tumor-Infiltrating,
pubmed-meshheading:7906140-Melanoma,
pubmed-meshheading:7906140-Molecular Sequence Data,
pubmed-meshheading:7906140-RNA, Messenger,
pubmed-meshheading:7906140-Transfection,
pubmed-meshheading:7906140-Tumor Cells, Cultured
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pubmed:year |
1993
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pubmed:articleTitle |
Tumor escape mechanisms from immunosurveillance: induction of unresponsiveness in a specific MHC-restricted CD4+ human T cell clone by the autologous MHC class II+ melanoma.
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pubmed:affiliation |
Institute of Dermatology, University of Würzburg, Germany.
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pubmed:publicationType |
Journal Article
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