Source:http://linkedlifedata.com/resource/pubmed/id/14871250
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2004-2-11
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| pubmed:abstractText |
Minor histocompatibility antigens (mHAs) are major histocompatibility complex (MHC)-associated peptides, which trigger T-cell responses that mediate graft versus host disease (GVHD) and graft versus leukaemia effects. We recently identified a new mHA epitope, termed ACC-1, which is presented by HLA-A*2402 and encoded by BCL2A1, whose expression is restricted to haematopoietic cells including leukaemic cells. HLA-A24/ACC-1 tetramer detected the presence of ACC-1-specific CD8+ cells in the peripheral blood of a patient up to 7 months following transplantation, and these tetramer-positive cells were expandable in vitro by ACC-1 peptide stimulation. A retrospective analysis of 320 patients with HLA-A*2402 who had received a human leucocyte antigen (HLA) genotypically matched unrelated donor through the Japan Marrow Donor Programme was conducted to determine whether ACC-1 disparity is associated with adverse clinical outcomes such as GVHD. Among these patients, ACC-1 disparity was detected in 55 (17.2%) donor/recipient pairs. After adjusting for known risk factors, the hazard ratios or odds ratios of acute and chronic GVHD, relapse and disease-free survival were not statistically different between patients receiving ACC-1 compatible and incompatible transplantation. These data suggest that disparity of haematopoietic cell-specific mHA, ACC-1, is unlikely at least to augment GVHD, and that T cells specific for ACC-1 may also be used for immunotherapy of recurring leukaemia without GVHD.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0007-1048
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
124
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
629-35
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:14871250-Adolescent,
pubmed-meshheading:14871250-Adult,
pubmed-meshheading:14871250-Bone Marrow Transplantation,
pubmed-meshheading:14871250-Child,
pubmed-meshheading:14871250-Child, Preschool,
pubmed-meshheading:14871250-Epitopes,
pubmed-meshheading:14871250-Female,
pubmed-meshheading:14871250-Genes, BRCA2,
pubmed-meshheading:14871250-Graft vs Host Disease,
pubmed-meshheading:14871250-Graft vs Leukemia Effect,
pubmed-meshheading:14871250-HLA-A Antigens,
pubmed-meshheading:14871250-HLA-A24 Antigen,
pubmed-meshheading:14871250-Hematologic Neoplasms,
pubmed-meshheading:14871250-Humans,
pubmed-meshheading:14871250-Infant,
pubmed-meshheading:14871250-Male,
pubmed-meshheading:14871250-Middle Aged,
pubmed-meshheading:14871250-Minor Histocompatibility Antigens,
pubmed-meshheading:14871250-Polymorphism, Genetic,
pubmed-meshheading:14871250-Retrospective Studies,
pubmed-meshheading:14871250-Risk Factors,
pubmed-meshheading:14871250-T-Lymphocytes
|
| pubmed:year |
2004
|
| pubmed:articleTitle |
Clinical relevance of a newly identified HLA-A24-restricted minor histocompatibility antigen epitope derived from BCL2A1, ACC-1, in patients receiving HLA genotypically matched unrelated bone marrow transplant.
|
| pubmed:affiliation |
Division of Immunology, Aichi Cancer Centre Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|