Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1998-11-30
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-4971
pubmed:author
pubmed:copyrightInfo
Copyright 1998 by The American Society of Hematology
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3355-61
pubmed:dateRevised
2011-11-17
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
pubmed:year
1998
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.
pubmed:affiliation
First Department of Internal Medicine, Ehime University School of Medicine, Ehime, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't