| pubmed-article:20132662 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20132662 | lifeskim:mentions | umls-concept:C0024314 | lld:lifeskim |
| pubmed-article:20132662 | lifeskim:mentions | umls-concept:C2350463 | lld:lifeskim |
| pubmed-article:20132662 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:20132662 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:20132662 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:20132662 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20132662 | pubmed:dateCreated | 2010-2-5 | lld:pubmed |
| pubmed-article:20132662 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:abstractText | To clarify the difference between gene expression signature of Epstein-Barr virus (EBV)-positive gammadelta T-cell lymphoproliferative disorders (LPD) and those in normal gammadelta T-cells, we set out to determine gene expression profiling using three gammadelta T-cell lines derived from patients with EBV-positive gammadelta T-cell LPD. Gene expression profiling using an Affymetrix Genechip revealed a unique gene expression pattern of NK cell receptors in gammadelta T-LPD cell lines. Genes encoding killer cell lectin-like receptors (KLR), such as KLRG1 and KLRB1 (CD161), were generally low in gammadelta T-LPD cell lines, while killer cell immunoglobulin-like receptors varied among cell lines. In addition, expression of CD161 surface antigen was found to be remarkably decreased in gammadelta T-LPD cell lines by flow cytometric analysis. We conclude that gammadelta T-cell expansion in EBV-positive gammadelta T-LPD is in part due to inappropriate expression of the NK cell receptors which related to impaired function cytotoxic T cells. | lld:pubmed |
| pubmed-article:20132662 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20132662 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20132662 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20132662 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:20132662 | pubmed:issn | 1607-8454 | lld:pubmed |
| pubmed-article:20132662 | pubmed:author | pubmed-author:ZhangYuY | lld:pubmed |
| pubmed-article:20132662 | pubmed:author | pubmed-author:OhyashikiKazu... | lld:pubmed |
| pubmed-article:20132662 | pubmed:author | pubmed-author:OhyashikiJunk... | lld:pubmed |
| pubmed-article:20132662 | pubmed:author | pubmed-author:ShimizuNorioN | lld:pubmed |
| pubmed-article:20132662 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20132662 | pubmed:volume | 15 | lld:pubmed |
| pubmed-article:20132662 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20132662 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20132662 | pubmed:pagination | 43-7 | lld:pubmed |
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| pubmed-article:20132662 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20132662 | pubmed:articleTitle | Aberrant expression of NK cell receptors in Epstein-Barr virus-positive gammadelta T-cell lymphoproliferative disorders. | lld:pubmed |
| pubmed-article:20132662 | pubmed:affiliation | First Department of Internal Medicine, Tokyo Medical University, Japan. | lld:pubmed |
| pubmed-article:20132662 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20132662 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
