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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1998-11-30
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pubmed:abstractText |
Although it is well known that CD8(+) cytotoxic T lymphocytes (CTLs) play an important role in the suppression of cancer cell growth, the significance of CD4(+) CTLs in resistance to cancer is obscure. In an attempt to elucidate the role of CD4(+) CTLs in immunosurveillance of chronic myelogenous leukemia (CML), we examined the immunologic functions of bcr-abl b3a2 fusion peptide-specific CD4(+) CTL clones. Seven CD4(+) T-cell clones that responded to stimulation with b3a2 peptide, but not with b2a2 peptide or physiological counterparts bcr b3b4 and abl 1A-a2 peptides, were established from two healthy individuals. Restriction elements of these clones were HLA-DRB1*0901. These CD4(+) T-cell clones exhibited b3a2 peptide-specific and HLA-DRB1*0901-restricted cytotoxicity and produced interleukin-3 (IL-3), IL-4, IL-10, interferon-gamma, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor in response to bcr-abl peptide stimulation, indicating they were Th0 clones. The numbers of HLA-DRB1*0901-positive b3a2, but not those of b2a2-positive or HLA-DRB1*0901-negative CML cell colonies increased when CML cells were cultured with b3a2-specific CD4(+) CTL clones. These data suggest that bcr-abl-specific CD4(+) CTLs recognize CML cells in an antigen-specific and HLA-DR-restricted manner, and that they do not inhibit, but in fact augment, CML cell growth.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DR Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DR alpha-Chains,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-DRB1 Chains,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1998 by The American Society of Hematology
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
92
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3355-61
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9787173-Amino Acid Sequence,
pubmed-meshheading:9787173-Animals,
pubmed-meshheading:9787173-Antigen Presentation,
pubmed-meshheading:9787173-CD4-Positive T-Lymphocytes,
pubmed-meshheading:9787173-Fusion Proteins, bcr-abl,
pubmed-meshheading:9787173-HLA-DR Antigens,
pubmed-meshheading:9787173-HLA-DR alpha-Chains,
pubmed-meshheading:9787173-HLA-DRB1 Chains,
pubmed-meshheading:9787173-Humans,
pubmed-meshheading:9787173-Immunologic Surveillance,
pubmed-meshheading:9787173-L Cells (Cell Line),
pubmed-meshheading:9787173-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:9787173-Mice,
pubmed-meshheading:9787173-Molecular Sequence Data,
pubmed-meshheading:9787173-Peptide Fragments,
pubmed-meshheading:9787173-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:9787173-Transfection,
pubmed-meshheading:9787173-Tumor Stem Cell Assay
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pubmed:year |
1998
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pubmed:articleTitle |
CD4(+) cytotoxic T-cell clones specific for bcr-abl b3a2 fusion peptide augment colony formation by chronic myelogenous leukemia cells in a b3a2-specific and HLA-DR-restricted manner.
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pubmed:affiliation |
First Department of Internal Medicine, Ehime University School of Medicine, Ehime, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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