Source:http://linkedlifedata.com/resource/pubmed/id/15077221
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0015219,
umls-concept:C0018133,
umls-concept:C0026189,
umls-concept:C0085358,
umls-concept:C0439851,
umls-concept:C1332714,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1527148,
umls-concept:C1552596,
umls-concept:C1706438,
umls-concept:C1947931,
umls-concept:C2003874,
umls-concept:C2698600
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pubmed:issue |
4
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pubmed:dateCreated |
2004-4-12
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pubmed:abstractText |
Graft-versus-host disease (GVHD) can be induced in lethally irradiated mice after allogeneic bone marrow transplantation between major histocompatibility complex-matched strains expressing multiple minor histocompatibility antigen differences. In the B6 --> BALB.B irradiation model, both CD4(+) and CD8(+) donor T cells have the capacity to mediate lethal GVHD. Previously, CDR3-size spectratyping was used to analyze these T-cell responses at a single early time point (day 5) after transplantation and revealed clonal or oligoclonal expansions of the V beta 2, 4, and 6 to 14 families for the CD4(+) response and of the V beta 4, 6, 8 to 11, and 14 families for the B6 CD8(+) response. Appropriate positive selection of these T-cell receptor V beta-skewed CD4(+) and CD8(+) T-cell subsets and their subsequent transfer into lethally irradiated BALB.B recipients resulted in fatal GVHD induction. In contrast, BALB.B mice transplanted with nonskewed V beta CD4(+) T cells survived, with minimal symptoms of GVHD. This study was undertaken to investigate the evolution of the donor/antihost minor histocompatibility antigen T-cell repertoire responses throughout the course of GVHD development. The results indicated that a number of V beta families were consistently involved throughout the course of GVHD, whereas some V beta families exhibited skewed expansions only in either the early or late stages of disease. In addition, sequence analysis of relevant representative skewed CDR3 bands from the CD4(+) V beta 11(+) and the CD8(+) V beta 14(+) families, both of which exhibited strong consistent responses, demonstrated increased use of the J beta 2.5 and J beta 2.4 segments, respectively, thus identifying the T-cell receptor specificities involved.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1083-8791
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
224-35
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15077221-Animals,
pubmed-meshheading:15077221-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15077221-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15077221-DNA Fingerprinting,
pubmed-meshheading:15077221-Genes, T-Cell Receptor beta,
pubmed-meshheading:15077221-Graft vs Host Disease,
pubmed-meshheading:15077221-Lymphocyte Activation,
pubmed-meshheading:15077221-Mice,
pubmed-meshheading:15077221-Minor Histocompatibility Antigens,
pubmed-meshheading:15077221-Polymerase Chain Reaction,
pubmed-meshheading:15077221-Receptor-CD3 Complex, Antigen, T-Cell,
pubmed-meshheading:15077221-Transplantation Conditioning
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pubmed:year |
2004
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pubmed:articleTitle |
Evolution of responding CD4+ and CD8+ T-cell repertoires during the development of graft-versus-host disease directed to minor histocompatibility antigens.
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pubmed:affiliation |
Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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