| pubmed-article:19032228 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19032228 | lifeskim:mentions | umls-concept:C0010823 | lld:lifeskim |
| pubmed-article:19032228 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:19032228 | lifeskim:mentions | umls-concept:C0022671 | lld:lifeskim |
| pubmed-article:19032228 | lifeskim:mentions | umls-concept:C2350463 | lld:lifeskim |
| pubmed-article:19032228 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:19032228 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:19032228 | pubmed:dateCreated | 2008-11-26 | lld:pubmed |
| pubmed-article:19032228 | pubmed:abstractText | Cytomegalovirus (CMV) infection is the most common viral complication after solid organ transplantation (SOT). Whilst current immunosuppression is known to impair antiviral-specific T-cell immunity in SOT, a potential role for natural killer (NK) cells not affected by immunosuppressive therapy remains to be determined. To address this, we compared the genotype of the NK immunoglobulin-like receptor (KIR) genes and their HLA cognate ligands to the rate of CMV infection in 196 kidney transplant recipients. We have shown that the absence of the HLA-C ligand for inhibitory KIR and the presence of activating KIR genes in the recipients were both associated with a lower rate of CMV infection after transplantation. In a cohort of 17 recipients with acute CMV infection, NK cells were phenotyped over a period of time after diagnosis by their expression profile of C-type lectin receptors and capacity to secrete IFN-gamma. The increased expression of the activating C-type lectin receptors NKG2C and NKG2D was paralleled by the decreased IFN-gamma secretion during the early phase of CMV infection. In conclusion, our findings suggest that KIR/HLA genotype and expression of NKG2C and NKG2D might play a significant role in regulating NK cell function and anti-CMV immunity after kidney transplantation. | lld:pubmed |
| pubmed-article:19032228 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19032228 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19032228 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19032228 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19032228 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:19032228 | pubmed:issn | 1600-6143 | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:VillardJJ | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:MartinP YPY | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:BernesJJ | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:KaiserLL | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:BuhlerLL | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:TiercyJ MJM | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:SeebachJ DJD | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:HadayaKK | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:Ferrari-Lacra... | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:BandelierCC | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:de RhamCC | lld:pubmed |
| pubmed-article:19032228 | pubmed:author | pubmed-author:JendlySS | lld:pubmed |
| pubmed-article:19032228 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19032228 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:19032228 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19032228 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19032228 | pubmed:pagination | 2674-83 | lld:pubmed |
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| pubmed-article:19032228 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:19032228 | pubmed:articleTitle | Natural killer cell receptor repertoire and their ligands, and the risk of CMV infection after kidney transplantation. | lld:pubmed |
| pubmed-article:19032228 | pubmed:affiliation | Service of Nephrology, Geneva University Hospital and Medical School, Switzerland. | lld:pubmed |
| pubmed-article:19032228 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19032228 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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