rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2007-11-5
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pubmed:abstractText |
Although the linkage between innate and adaptive immunity in transplantation has been recognized, the mechanisms underlying this cooperation remain to be fully elucidated. In this study, we show that early "danger" signals associated with transplantation lead to rapid up-regulation of NKG2D ligands. A second wave of NKG2D ligand up-regulation is mediated by the adaptive immune response to allografts. Treatment with an Ab to NKG2D was highly effective in preventing CD28-independent rejection of cardiac allografts. Notably, NKG2D blockade did not deplete CD8(+) T cells or NK1.1(+) cells nor affect their migration to the allografts. These results establish a functional role of NKG2D and its ligands in the rejection of solid organ transplants.
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pubmed:grant |
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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/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Klrb1c protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Klrk1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Natural Killer Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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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 |
179
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6416-20
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17982029-Animals,
pubmed-meshheading:17982029-Antibodies,
pubmed-meshheading:17982029-Antigens, CD28,
pubmed-meshheading:17982029-Antigens, Ly,
pubmed-meshheading:17982029-Antigens, Surface,
pubmed-meshheading:17982029-CD8-Positive T-Lymphocytes,
pubmed-meshheading:17982029-Graft Rejection,
pubmed-meshheading:17982029-Heart Transplantation,
pubmed-meshheading:17982029-Immunity, Innate,
pubmed-meshheading:17982029-Lectins, C-Type,
pubmed-meshheading:17982029-Ligands,
pubmed-meshheading:17982029-Mice,
pubmed-meshheading:17982029-Mice, Inbred BALB C,
pubmed-meshheading:17982029-NK Cell Lectin-Like Receptor Subfamily B,
pubmed-meshheading:17982029-NK Cell Lectin-Like Receptor Subfamily K,
pubmed-meshheading:17982029-Receptors, Immunologic,
pubmed-meshheading:17982029-Receptors, Natural Killer Cell,
pubmed-meshheading:17982029-Transplantation, Homologous,
pubmed-meshheading:17982029-Up-Regulation
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pubmed:year |
2007
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pubmed:articleTitle |
The activating immunoreceptor NKG2D and its ligands are involved in allograft transplant rejection.
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pubmed:affiliation |
Transplantation Research Laboratory, Division of Transplantation, Department of Surgery, University of California, San Francisco, CA 94143, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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