Source:http://linkedlifedata.com/resource/pubmed/id/11300482
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3 Suppl
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| pubmed:dateCreated |
2001-4-12
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| pubmed:abstractText |
We have reported previously that MUC1 transgenic mice with spontaneous tumors of the pancreas (designated MET) naturally develop MHC class I-restricted, MUC1-specific CTLs as tumors progress (P. Mukherjee et al., J. Immunol., 165: 3451-3460, 2000). From these MET mice, we have isolated, expanded, and cloned naturally occurring MUC1-specific CTLs in vitro. In this report, we show that the CTL line is predominantly CD8+ T cells and expresses T-cell receptor Vbeta chains 5.1/5.2, 11, 13, and 2 and Valpha chains 2, 8.3, 3.2, and 11.1/11.2. These CTLs recognize several epitopes on the MUC1 tandem repeat with highest affinity to APGSTAPPA. The CTL clone, on the other hand, is 100% CD8+ cells and expresses a single Vbeta chain of 5.1/5.2 and Valpha2. It recognizes only the H-2Db class I-restricted epitope of MUC1, APGSTAPPA. When adoptively transferred, the CTLs were effective in eradicating MUC1-expressing injected tumor cells including mammary gland cells (C57mg) and B16 melanomas. These results suggest that MUC1-specific CTLs are capable of possibly preventing, or at least substantially delaying, MUC1-expressing tumor formation. To our knowledge, this is the first evidence that demonstrates that the naturally occurring MUC1-specific CTLs isolated from one tumor model has antitumor effects on other MUC1-expressing tumors in vivo. Therefore, our data confirm that MUC1 is an important tumor rejection antigen and can serve as a target for immunotherapy.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Mucin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
1078-0432
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
7
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
848s-855s
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:11300482-Adoptive Transfer,
pubmed-meshheading:11300482-Animals,
pubmed-meshheading:11300482-CD8-Positive T-Lymphocytes,
pubmed-meshheading:11300482-Cell Line,
pubmed-meshheading:11300482-Cell Separation,
pubmed-meshheading:11300482-Epitopes,
pubmed-meshheading:11300482-Flow Cytometry,
pubmed-meshheading:11300482-Humans,
pubmed-meshheading:11300482-Interferon-gamma,
pubmed-meshheading:11300482-Melanoma, Experimental,
pubmed-meshheading:11300482-Mice,
pubmed-meshheading:11300482-Mice, Transgenic,
pubmed-meshheading:11300482-Mucin-1,
pubmed-meshheading:11300482-Peptides,
pubmed-meshheading:11300482-Polymerase Chain Reaction,
pubmed-meshheading:11300482-Receptors, Antigen, T-Cell,
pubmed-meshheading:11300482-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:11300482-Time Factors
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| pubmed:year |
2001
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| pubmed:articleTitle |
MUC1-specific cytotoxic T lymphocytes eradicate tumors when adoptively transferred in vivo.
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| pubmed:affiliation |
Department of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, Arizona 85259, USA.
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| pubmed:publicationType |
Journal Article
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