Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2007-11-5
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
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
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6416-20
pubmed:dateRevised
2008-11-21
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
pubmed:year
2007
pubmed:articleTitle
The activating immunoreceptor NKG2D and its ligands are involved in allograft transplant rejection.
pubmed:affiliation
Transplantation Research Laboratory, Division of Transplantation, Department of Surgery, University of California, San Francisco, CA 94143, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural