Source:http://linkedlifedata.com/resource/pubmed/id/16380474
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
2005-12-28
|
| pubmed:abstractText |
A role of natural killer T (NKT) cells in transplant rejection remains unknown. Here, we determined whether NKT cells participate in rejection of islet allografts, using NKT cell-deficient mice. Survival of islet allografts in streptozotocin-induced diabetic CD1d(-/-) mice or Valpha14 NKT cell(-/-) mice was significantly prolonged without immunosuppression when grafted into the liver, but not beneath the kidney capsule, compared with wild-type mice. Acceptance of intrahepatic islet allografts was achieved in CD1d(-/-) mice by a subtherapeutic dose of rapamycin, which was abrogated in conjunction with the transfer of hepatic mononuclear cells from wild-type, but not from CD1d(-/-), mice at islet transplantation. The second islet grafts from a donor-specific, but not from a third-party, strain in CD1d(-/-) mice bearing functional islet allografts were accepted without immunosuppression at 120 days after the initial transplantation. These findings demonstrate that NKT cells play a significant role in rejection of islet allografts in the liver of mice, but that NKT cells are not essential for induction of donor-specific unresponsiveness in this model. The current study indicates that NKT cells might be considered as a target for intervention to prevent islet allograft rejection when the liver is the site of transplantation.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0012-1797
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| pubmed:author |
pubmed-author:IkedaSeiyoS,
pubmed-author:MatsuokaNobuhideN,
pubmed-author:NabeyamaKentarohK,
pubmed-author:NakanoMasahikoM,
pubmed-author:NakayamaToshinoriT,
pubmed-author:OnoJunkoJ,
pubmed-author:SatohMasayukiM,
pubmed-author:TanakaMasaoM,
pubmed-author:TaniguchiMasaruM,
pubmed-author:ToyofukuAtsushiA,
pubmed-author:YasunamiYohichiY
|
| pubmed:issnType |
Print
|
| pubmed:volume |
55
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
34-9
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:16380474-Adoptive Transfer,
pubmed-meshheading:16380474-Animals,
pubmed-meshheading:16380474-Antigens, CD1,
pubmed-meshheading:16380474-Gene Deletion,
pubmed-meshheading:16380474-Graft Rejection,
pubmed-meshheading:16380474-Interferon-gamma,
pubmed-meshheading:16380474-Islets of Langerhans,
pubmed-meshheading:16380474-Islets of Langerhans Transplantation,
pubmed-meshheading:16380474-Kidney,
pubmed-meshheading:16380474-Killer Cells, Natural,
pubmed-meshheading:16380474-Liver,
pubmed-meshheading:16380474-Male,
pubmed-meshheading:16380474-Mice,
pubmed-meshheading:16380474-Mice, Inbred BALB C,
pubmed-meshheading:16380474-Mice, Inbred C3H,
pubmed-meshheading:16380474-Mice, Inbred C57BL,
pubmed-meshheading:16380474-Receptors, Interleukin-2,
pubmed-meshheading:16380474-Sirolimus,
pubmed-meshheading:16380474-Up-Regulation
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Natural killer T-cells participate in rejection of islet allografts in the liver of mice.
|
| pubmed:affiliation |
Department of Surgery I, Fukuoka University School of Medicine, 7-45-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|