| pubmed-article:20439722 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20439722 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
| pubmed-article:20439722 | lifeskim:mentions | umls-concept:C0254610 | lld:lifeskim |
| pubmed-article:20439722 | lifeskim:mentions | umls-concept:C0022688 | lld:lifeskim |
| pubmed-article:20439722 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:20439722 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:20439722 | lifeskim:mentions | umls-concept:C0002085 | lld:lifeskim |
| pubmed-article:20439722 | pubmed:issue | 20 | lld:pubmed |
| pubmed-article:20439722 | pubmed:dateCreated | 2010-5-20 | lld:pubmed |
| pubmed-article:20439722 | pubmed:abstractText | The nonobese diabetic (NOD) mouse strain has a genetic deficiency in natural killer (NK) cells. This defect underlies this strain's utility in several experimental settings; in particular, it promotes engraftment of human tissue in NOD hosts during the generation of "humanized" mouse models. We have mapped the major NK-cell defect in the NOD vs. C57BL/6 (B6) strain to an inadequately expressed Il15 allele. Treatment of NOD mice with a reagent that specifically enhances interleukin (IL)-15 bioavailability normalized NK-cell numbers and activity in the absence of nonspecific stimulation. These findings raise the possibility of exploiting reagents that impact the IL-15 receptor pathway to facilitate construction of humanized mouse models on non-NOD genetic backgrounds. | lld:pubmed |
| pubmed-article:20439722 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20439722 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20439722 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20439722 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20439722 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20439722 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20439722 | pubmed:month | May | lld:pubmed |
| pubmed-article:20439722 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:20439722 | pubmed:author | pubmed-author:SuwanaiHirots... | lld:pubmed |
| pubmed-article:20439722 | pubmed:author | pubmed-author:BenoistChrist... | lld:pubmed |
| pubmed-article:20439722 | pubmed:author | pubmed-author:MathisDianeD | lld:pubmed |
| pubmed-article:20439722 | pubmed:author | pubmed-author:WilcoxMartha... | lld:pubmed |
| pubmed-article:20439722 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20439722 | pubmed:day | 18 | lld:pubmed |
| pubmed-article:20439722 | pubmed:volume | 107 | lld:pubmed |
| pubmed-article:20439722 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20439722 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20439722 | pubmed:pagination | 9305-10 | lld:pubmed |
| pubmed-article:20439722 | pubmed:dateRevised | 2010-11-22 | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:meshHeading | pubmed-meshheading:20439722... | lld:pubmed |
| pubmed-article:20439722 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20439722 | pubmed:articleTitle | A defective Il15 allele underlies the deficiency in natural killer cell activity in nonobese diabetic mice. | lld:pubmed |
| pubmed-article:20439722 | pubmed:affiliation | Section on Immunology and Immunogenetics, Joslin Diabetes Center, Boston, MA 02215, USA. | lld:pubmed |
| pubmed-article:20439722 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20439722 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:20439722 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:16168 | entrezgene:pubmed | pubmed-article:20439722 | lld:entrezgene |
| entrez-gene:111364 | entrezgene:pubmed | pubmed-article:20439722 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:20439722 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20439722 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:20439722 | lld:pubmed |
