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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1996-3-6
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pubmed:abstractText |
Targeted disruption of the CD8 gene results in a profound block in cytotoxic T cell (CTL) development. Since CTL are major histocompatibility complex (MHC) class I restricted, we addressed the question of whether CD8-/- mice can reject MHC class I-disparate allografts. Studies have previously shown that skin allografts are rejected exclusively by T cells. We therefore used the skin allograft model to answer our question and grafted CD8-/- mice with skins from allogeneic mice deficient in MHC class II or in MHC class I (MHC-I or MHC-II-disparate, respectively). CD8-/- mice rejected MHC-I-disparate skin rapidly even if they were depleted of CD4+ cells in vivo (and were thus deficient in CD4+ and CD8+ T cells). By contrast, CD8+/+ controls depleted of CD4+ and CD8+ T cells in vivo accepted the MHC-I-disparate skin. Following MHC-I, but not MHC-II stimulation, allograft-specific cytotoxic activity was detected in CD8-/- mice even after CD4 depletion. A population expanded in both the lymph nodes and the thymus of grafted CD8-/- animals which displayed a CD4-8-3intermediateTCR alpha/betaintermediate phenotype. Indeed its T cell receptor (TCR) density was lower than that of CD4+ cells in CD8-/- mice or of CD8+ cells in CD8+/+ mice. Our data suggest that this CD4-8- T cell population is responsible for the CTL function we have observed. Therefore, MHC class I-restricted CTL can be generated in CD8-/- mice following priming with MHC class I antigens in vivo. The data also suggest that CD8 is needed to up-regulate TCR density during thymic maturation. Thus, although CD8 plays a major role in the generation of CTL, it is not absolutely required.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0014-2980
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
213-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8566069-Animals,
pubmed-meshheading:8566069-Antigens, CD4,
pubmed-meshheading:8566069-Antigens, CD8,
pubmed-meshheading:8566069-Cytotoxicity, Immunologic,
pubmed-meshheading:8566069-Graft Rejection,
pubmed-meshheading:8566069-H-2 Antigens,
pubmed-meshheading:8566069-Histocompatibility Antigens Class II,
pubmed-meshheading:8566069-Immunophenotyping,
pubmed-meshheading:8566069-Lymphocyte Activation,
pubmed-meshheading:8566069-Mice,
pubmed-meshheading:8566069-Mice, Mutant Strains,
pubmed-meshheading:8566069-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:8566069-Skin Transplantation,
pubmed-meshheading:8566069-T-Lymphocytes, Cytotoxic
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pubmed:year |
1996
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pubmed:articleTitle |
CD4-negative cytotoxic T cells with a T cell receptor alpha/beta intermediate expression in CD8-deficient mice.
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pubmed:affiliation |
R.W. Johnson Pharmaceutical Research Institute, Toronto, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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