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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1989-3-13
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pubmed:abstractText |
Previous studies have indicated that the frequency of murine CTL precursors (CTLp) for human class I molecules is one to two orders of magnitude lower than that for murine class I alloantigens, and that this is due to species-specific structural differences between these molecules. Transgenic mice expressing the human class I MHC Ag HLA-A2.1 were used to examine changes in the frequency of class I HLA-specific precursors after T cell differentiation in an HLA-A2.1 positive environment. The HLA-A2.1 gene product was expressed at levels comparable to those of the endogenous H-2Db molecule in thymus, bone marrow, and spleen. By limiting dilution analysis, it was observed that the frequencies of CTLp in transgenic mice responding to the human alloantigens HLA-B7 or HLA-A2.2 were comparable to or lower than those in normal C57BL/6 mice, regardless of whether the Ag was presented on human or murine cells. Thus, expression of a human class I molecule in these animals did not result in an expansion of the number of CTLp specific for other human class I Ag. In addition, the frequency of HLA-A2.1-restricted, influenza specific CTLp was substantially lower than the frequency of H-2b restricted CTLp, indicating a poor utilization of HLA-A2.1 as a restricting element. Finally, the frequencies of CTLp for HLA-A2.1 expressed on syngeneic murine tumor cells were decreased significantly. Thus, expression of HLA-A2.1 in these animals appeared to induced tolerance to this Ag. Interestingly, however, these mice were not tolerant to the HLA-A2.1 molecule expressed on human cells. This indicates that the HLA-A2.1 associated epitopes expressed on murine and human cells differ and suggests that, under these circumstances, HLA-A2.1 acts as a restricting element for human nominal Ag. These results are discussed in the context of current models of T cell repertoire development.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-A Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B7 Antigen
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
142
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1366-71
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2464645-Animals,
pubmed-meshheading:2464645-Cytotoxicity, Immunologic,
pubmed-meshheading:2464645-Epitopes,
pubmed-meshheading:2464645-H-2 Antigens,
pubmed-meshheading:2464645-HLA-A Antigens,
pubmed-meshheading:2464645-HLA-B Antigens,
pubmed-meshheading:2464645-HLA-B7 Antigen,
pubmed-meshheading:2464645-Humans,
pubmed-meshheading:2464645-Immune Tolerance,
pubmed-meshheading:2464645-Influenza A virus,
pubmed-meshheading:2464645-Leukocyte Count,
pubmed-meshheading:2464645-Lymphoid Tissue,
pubmed-meshheading:2464645-Mice,
pubmed-meshheading:2464645-Mice, Transgenic,
pubmed-meshheading:2464645-Species Specificity,
pubmed-meshheading:2464645-Stem Cells,
pubmed-meshheading:2464645-T-Lymphocytes, Cytotoxic
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pubmed:year |
1989
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pubmed:articleTitle |
Cytotoxic T cell responses in HLA-A2.1 transgenic mice. Recognition of HLA alloantigens and utilization of HLA-A2.1 as a restriction element.
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pubmed:affiliation |
Department of Surgery, University of Virginia Medical Center, Charlottesville 22908.
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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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