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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1996-5-29
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pubmed:abstractText |
B7.75-84, a 10-amino-acid peptide derived from the HLA-B7 molecule, prolongs rat heterotopic cardiac allograft survival time (GST) when used with cyclosporine in the Lewis-to-ACI strain combination. We evaluated the ability of B7.75-84 to prolong GST in other strain combinations without cyclosporine and studied the effect of B7.75-84 on the immune response in the Wistar-Furth (WF)-to-ACI strain combination. GST was markedly prolonged in most low-responder (ACI) recipients but only slightly prolonged in the high-responder (Lewis) recipient. Cytotoxic T lymphocyte (CTL) and helper T lymphocyte (HTL) limiting dilution assays (LDA) were performed 10 days after cardiac allografts from WF donors were placed in ACI recipients treated with B7.75-84. HTL-LDA assays at 10 days posttransplant showed a slight decrease in HTL precursor frequency and a decrease in their IL-2 production in B7.75-84 treated recipients with prolonged GST in response to donor antigen as well as third-party (Lewis) antigen. CTL-LDA assays at day 10 showed no difference in CTL precursor frequency among treated recipients but did show a significant decrease in CTL killing activity against donor cells in recipients with prolonged GST. No significant difference in CTL killing activity was seen against third- party cells. Antibody analysis was performed at day 8 in treated recipients. Serum from B7.75-84-treated recipients with prolonged graft survival generally showed no detectable IgG antibody response against donor MHC class I antigen. All B7.75-84 treated recipients showed a strong IgM response against donor antigen regardless of allograft outcome. Our results suggest that the immunosuppressive effect of B7.75-84 in rats is greater using a low-responder RT1 haplotype. Furthermore, B7.75-84 induces a nonspecific decrease in HTL function while producing a donor-specific decrease in CTL function and a diminished antidonor MHC class I IgG response.
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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 |
0041-1337
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
61
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1222-8
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pubmed:dateRevised |
2003-11-14
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pubmed:meshHeading |
pubmed-meshheading:8610422-Animals,
pubmed-meshheading:8610422-Graft Rejection,
pubmed-meshheading:8610422-Heart Transplantation,
pubmed-meshheading:8610422-Histocompatibility Antigens Class I,
pubmed-meshheading:8610422-Immunosuppressive Agents,
pubmed-meshheading:8610422-Male,
pubmed-meshheading:8610422-Peptide Fragments,
pubmed-meshheading:8610422-Rats,
pubmed-meshheading:8610422-Rats, Inbred ACI,
pubmed-meshheading:8610422-Rats, Inbred F344,
pubmed-meshheading:8610422-Rats, Inbred Lew,
pubmed-meshheading:8610422-Transplantation, Homologous
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pubmed:year |
1996
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pubmed:articleTitle |
Immunosuppressive effects of an HLA class I-derived peptide in a rat cardiac allograft model.
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pubmed:affiliation |
University of Wisconsin Medical School, Madison 53792, USA.
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pubmed:publicationType |
Journal Article
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