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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1993-2-9
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pubmed:abstractText |
Monoclonal antibodies directed against different T cell subpopulations have been used in several rodent models of transplantation to induce long-term unresponsiveness to allografts by a variety of mechanisms. To investigate whether different mechanisms may be operative when different regimens of mAb therapy are used, we studied the effects of various combinations of anti-T-cell antibody treatment on the induction of tolerance in a mouse islet allograft model. Anti-CD4 mAb alone, anti-CD8 mAb alone, anti-CD4 mAb plus anti-CD8 mAb, and anti-Thy1.2 mAb alone were given at the time of engraftment. Only the anti-CD4 mAb and the anti-CD4 mAb plus anti-CD8 mAb regimens were successful in inducing permanent unresponsiveness to islet allografts. We have previously shown that anti-CD4 mAb alone induces permanent unresponsiveness to islet allografts by a mechanism of clonal anergy, as demonstrated by unresponsiveness of potentially alloreactive T cells to anti-T-cell receptor-specific cross-linking. Interestingly, the potentially alloreactive T cell subsets of recipient mice (V beta 5+ and V beta 11+) made unresponsive to islet allografts by anti-CD4 mAb plus anti-CD8 mAb therapy were not found to be anergic using the same assay. Differences between the repopulation kinetics of CD8+ T cells of anti-CD4 mAb plus anti-CD8 mAb treated recipient mice, which accepted islet allografts, and anti-Thy1.2 treated recipient mice, which rejected islet allografts despite similar levels of initial T cell depletion, suggest that unresponsiveness to alloantigen may have been induced in anti-CD4 mAb plus anti-CD8 mAb treated recipients by clearance of donor passenger leukocytes during prolonged CD8+ T cell depletion.
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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 |
Jan
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pubmed:issn |
0041-1337
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
55
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
133-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8420037-Animals,
pubmed-meshheading:8420037-Antibodies, Monoclonal,
pubmed-meshheading:8420037-Antigenic Modulation,
pubmed-meshheading:8420037-Antigens, CD4,
pubmed-meshheading:8420037-Antigens, CD8,
pubmed-meshheading:8420037-Antilymphocyte Serum,
pubmed-meshheading:8420037-Graft Rejection,
pubmed-meshheading:8420037-Graft Survival,
pubmed-meshheading:8420037-Immune Tolerance,
pubmed-meshheading:8420037-Islets of Langerhans Transplantation,
pubmed-meshheading:8420037-Lymphocyte Activation,
pubmed-meshheading:8420037-Mice,
pubmed-meshheading:8420037-T-Lymphocytes,
pubmed-meshheading:8420037-Transplantation, Homologous
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pubmed:year |
1993
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pubmed:articleTitle |
Evidence that anti-CD8 abrogates anti-CD4-mediated clonal anergy but allows allograft survival in mice.
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pubmed:affiliation |
Department of Medicine, Stanford University School of Medicine, California 94305-5111.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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