Source:http://linkedlifedata.com/resource/pubmed/id/11673489
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2001-10-23
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pubmed:abstractText |
Many of the Ags recognized by human melanoma-reactive CTL are derived from proteins that are also expressed in melanocytes. The possibility of self-tolerance to these epitopes has led to questions about their utility for antitumor immunotherapy. To investigate the issue, we established a preclinical model based on transgenic mice expressing a recombinant HLA-A*0201 molecule and B16 melanoma transfected to express this molecule. HLA-A*0201-restricted epitopes from the melanocyte differentiation proteins (MDP) tyrosinase and gp100 are expressed in both tumor cells and melanocytes, and the former is associated with self-tolerance. However, adoptive transfer of tyrosinase or gp100-reactive CTL developed from tolerant mice delayed tumor outgrowth, as did immunization with MDP peptide-pulsed dendritic cells. Protection was enhanced by the use of peptide ligands containing conservative substitutions that were cross-reactive with the original Ags. These data establish that CTL populations reactive against MDP-derived self-Ags can be activated to mount effective antitumor immunity and strongly support their continued development for tumor immunotherapy in humans.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-A Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Monophenol Monooxygenase,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/SILV protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Si protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/gp100 Melanoma Antigen
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4853-60
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11673489-Animals,
pubmed-meshheading:11673489-Epitopes,
pubmed-meshheading:11673489-HLA-A Antigens,
pubmed-meshheading:11673489-Melanoma,
pubmed-meshheading:11673489-Membrane Glycoproteins,
pubmed-meshheading:11673489-Mice,
pubmed-meshheading:11673489-Mice, Inbred C57BL,
pubmed-meshheading:11673489-Mice, Transgenic,
pubmed-meshheading:11673489-Monophenol Monooxygenase,
pubmed-meshheading:11673489-Neoplasm Proteins,
pubmed-meshheading:11673489-gp100 Melanoma Antigen
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pubmed:year |
2001
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pubmed:articleTitle |
Immune responses to the HLA-A*0201-restricted epitopes of tyrosinase and glycoprotein 100 enable control of melanoma outgrowth in HLA-A*0201-transgenic mice.
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pubmed:affiliation |
Department of Microbiology and Carter Immunology Center, University of Virginia, Charlottesville, VA 22908, USA.
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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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