pubmed-article:19304328 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19304328 | lifeskim:mentions | umls-concept:C1868685 | lld:lifeskim |
pubmed-article:19304328 | lifeskim:mentions | umls-concept:C1416646 | lld:lifeskim |
pubmed-article:19304328 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
pubmed-article:19304328 | pubmed:issue | 1-2 | lld:pubmed |
pubmed-article:19304328 | pubmed:dateCreated | 2009-5-18 | lld:pubmed |
pubmed-article:19304328 | pubmed:abstractText | Several lines of evidence implicate CD56(bright) NK cells in the pathogenesis of multiple sclerosis (MS). This proposed immunoregulatory pathway involves already established susceptibility genes such as interleukin-2 receptor alpha (IL2RA) and interleukin-7 receptor (IL7R). We therefore investigated the CD56(bright) NK cell effector molecule KIR2DL4 for its involvement in genetic susceptibility to MS in a study population of 763 cases and 967 controls. Whereas 26% of the study population has a genotype corresponding to a lack of any functional membrane-bound form of the molecule, no association of the KIR2DL4 transmembrane alleles with susceptibility to MS was observed. | lld:pubmed |
pubmed-article:19304328 | pubmed:language | eng | lld:pubmed |
pubmed-article:19304328 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19304328 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19304328 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19304328 | pubmed:month | May | lld:pubmed |
pubmed-article:19304328 | pubmed:issn | 1872-8421 | lld:pubmed |
pubmed-article:19304328 | pubmed:author | pubmed-author:BoonenStevenS | lld:pubmed |
pubmed-article:19304328 | pubmed:author | pubmed-author:GorisAnA | lld:pubmed |
pubmed-article:19304328 | pubmed:author | pubmed-author:DuboisBénédic... | lld:pubmed |
pubmed-article:19304328 | pubmed:author | pubmed-author:NagelsGuyG | lld:pubmed |
pubmed-article:19304328 | pubmed:author | pubmed-author:DobosiRitaR | lld:pubmed |
pubmed-article:19304328 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19304328 | pubmed:day | 29 | lld:pubmed |
pubmed-article:19304328 | pubmed:volume | 210 | lld:pubmed |
pubmed-article:19304328 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19304328 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19304328 | pubmed:pagination | 113-5 | lld:pubmed |
pubmed-article:19304328 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:19304328 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19304328 | pubmed:articleTitle | KIR2DL4 (CD158d) polymorphisms and susceptibility to multiple sclerosis. | lld:pubmed |
pubmed-article:19304328 | pubmed:affiliation | Katholieke Universiteit Leuven, Belgium. An.Goris@med.kuleuven.be | lld:pubmed |
pubmed-article:19304328 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19304328 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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