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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2001-11-20
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pubmed:abstractText |
We have established H-2D(d)-transgenic (Tg) mice, in which H-2D(d) expression can be extinguished by Cre recombinase-mediated deletion of an essential portion of the transgene (Tg). NK cells adapted to the expression of the H-2D(d) Tg in H-2(b) mice and acquired reactivity to cells lacking H-2D(d), both in vivo and in vitro. H-2D(d)-Tg mice crossed to mice harboring an Mx-Cre Tg resulted in mosaic H-2D(d) expression. That abrogated NK cell reactivity to cells lacking D(d). In D(d) single Tg mice it is the Ly49A+ NK cell subset that reacts to cells lacking D(d), because the inhibitory Ly49A receptor is no longer engaged by its D(d) ligand. In contrast, Ly49A+ NK cells from D(d) x MxCre double Tg mice were unable to react to D(d)-negative cells. These Ly49A+ NK cells retained reactivity to target cells that were completely devoid of MHC class I molecules, suggesting that they were not anergic. Variegated D(d) expression thus impacts specifically missing D(d) but not globally missing class I reactivity by Ly49A+ NK cells. We propose that the absence of D(d) from some host cells results in the acquisition of only partial missing self-reactivity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cre recombinase,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Integrases,
http://linkedlifedata.com/resource/pubmed/chemical/Klra1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, NK Cell Lectin-Like,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/histocompatibility antigen H-2D(b)
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6256-62
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11714788-Animals,
pubmed-meshheading:11714788-Antigens, Ly,
pubmed-meshheading:11714788-Carrier Proteins,
pubmed-meshheading:11714788-Cells, Cultured,
pubmed-meshheading:11714788-Crosses, Genetic,
pubmed-meshheading:11714788-Cytomegalovirus,
pubmed-meshheading:11714788-Cytotoxicity, Immunologic,
pubmed-meshheading:11714788-Cytotoxicity Tests, Immunologic,
pubmed-meshheading:11714788-Gene Silencing,
pubmed-meshheading:11714788-Genetic Vectors,
pubmed-meshheading:11714788-H-2 Antigens,
pubmed-meshheading:11714788-Histocompatibility Antigens Class I,
pubmed-meshheading:11714788-Integrases,
pubmed-meshheading:11714788-Killer Cells, Natural,
pubmed-meshheading:11714788-Lectins, C-Type,
pubmed-meshheading:11714788-Lymphocyte Subsets,
pubmed-meshheading:11714788-Membrane Proteins,
pubmed-meshheading:11714788-Mice,
pubmed-meshheading:11714788-Mice, Inbred C57BL,
pubmed-meshheading:11714788-Mice, Inbred DBA,
pubmed-meshheading:11714788-Mice, Transgenic,
pubmed-meshheading:11714788-NK Cell Lectin-Like Receptor Subfamily A,
pubmed-meshheading:11714788-Receptors, Estrogen,
pubmed-meshheading:11714788-Receptors, NK Cell Lectin-Like,
pubmed-meshheading:11714788-Sequence Deletion,
pubmed-meshheading:11714788-Transgenes,
pubmed-meshheading:11714788-Viral Proteins
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pubmed:year |
2001
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pubmed:articleTitle |
Cre recombinase-mediated inactivation of H-2Dd transgene expression: evidence for partial missing self-recognition by Ly49A NK cells.
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pubmed:affiliation |
Ludwig Institute for Cancer Research, University of Lausanne, Epalinges, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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