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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1998-2-20
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pubmed:abstractText |
From the peripheral blood lymphocytes (PBLs) of melanoma patient SK29(AV) we have previously isolated 2 independent cytolytic T lymphocyte (CTL) clones (CTL7/147 and CTL13/211), which lysed autologous tumor cells in association with HLA-B45.1. As demonstrated here, both CTL clones were directed against melanocyte differentiation antigen Melan-A/MART-1, which also was recognized by HLA-A2.1-restricted CTLs from the same patient. By generating and transfecting 3'-deletion mutants of Melan-A/MART-1 cDNA, we localized its peptide-coding regions. The HLA-B45.1-presented peptides were derived from a hydrophobic region of the protein and largely overlapped the peptides recognized by CTLs from the same patient in association with HLA-A2.1. We determined the fine specificity of these CTL clones with synthetic peptides. CTL clone CTL7/147 recognized the 11-mer peptide AEEAAGIGILT (residues 24-34) at the lowest concentrations. The absence of threonine-34 abrogated the recognition by CTL7/147. The truncated peptide AEEAAGIGIL (residues 24-33) proved to be the optimal synthetic peptide for sensitization against lysis by CTL13/211. This indicated that C-terminal threonine-34 was not involved in binding to HLA-B45.1 but, rather, was part of the epitope for CTL7/147. HLA-B45.1-associated peptides of Melan-A/MART-1 were regularly processed and presented by other melanomas and other cell types. Three of 4 independent HLA-A2.1-restricted SK29-CTL clones recognized the 10-mer peptide EAAGIGILTV (residues 26-35) at 10- to 100-fold lower concentrations than the nonamer AAGIGILTV (residues 27-35), previously described as the common immunodominant peptide antigen for all known anti-Melan-A/MART-1 CTLs restricted by HLA-A2.1. Different melanoma peptide antigens currently are applied in therapeutic vaccination studies. Our findings emphasize that restricting to peptides of minimal length might exclude relevant T-cell epitopes.
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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/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-A2 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B45 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/MART-1 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/MLANA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0020-7136
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
30
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pubmed:volume |
75
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
451-8
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pubmed:dateRevised |
2011-5-23
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pubmed:meshHeading |
pubmed-meshheading:9455808-Amino Acid Sequence,
pubmed-meshheading:9455808-Animals,
pubmed-meshheading:9455808-Antigens, Neoplasm,
pubmed-meshheading:9455808-Base Sequence,
pubmed-meshheading:9455808-COS Cells,
pubmed-meshheading:9455808-DNA, Neoplasm,
pubmed-meshheading:9455808-Epitopes, T-Lymphocyte,
pubmed-meshheading:9455808-HLA-A2 Antigen,
pubmed-meshheading:9455808-HLA-B Antigens,
pubmed-meshheading:9455808-Humans,
pubmed-meshheading:9455808-MART-1 Antigen,
pubmed-meshheading:9455808-Melanoma,
pubmed-meshheading:9455808-Neoplasm Proteins,
pubmed-meshheading:9455808-Sequence Homology, Amino Acid,
pubmed-meshheading:9455808-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:9455808-Tumor Cells, Cultured
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pubmed:year |
1998
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pubmed:articleTitle |
Overlapping peptides of melanocyte differentiation antigen Melan-A/MART-1 recognized by autologous cytolytic T lymphocytes in association with HLA-B45.1 and HLA-A2.1.
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pubmed:affiliation |
I Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universität, Mainz, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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