| pubmed-article:15265789 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15265789 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:15265789 | lifeskim:mentions | umls-concept:C0022688 | lld:lifeskim |
| pubmed-article:15265789 | lifeskim:mentions | umls-concept:C0277784 | lld:lifeskim |
| pubmed-article:15265789 | lifeskim:mentions | umls-concept:C1335238 | lld:lifeskim |
| pubmed-article:15265789 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:15265789 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:15265789 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:15265789 | pubmed:dateCreated | 2004-11-4 | lld:pubmed |
| pubmed-article:15265789 | pubmed:abstractText | Interferon-gamma (IFN-gamma) production and cytolytic activity are 2 major biologic functions of natural killer (NK) cells that are important for innate immunity. We demonstrate here that these functions are compromised in human NK cells treated with peroxisome proliferator-activated-gamma (PPAR-gamma) ligands via both PPAR-gamma-dependent and -independent pathways due to variation in PPAR-gamma expression. In PPAR-gamma-null NK cells, 15-deoxy-Delta(12,14) prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, reduces IFN-gamma production that can be reversed by MG132 and/or chloroquine, and it inhibits cytolytic activity of NK cells through reduction of both conjugate formation and CD69 expression. In PPARgamma-positive NK cells, PPAR-gamma activation by 15d-PGJ(2) and ciglitazone (a synthetic ligand) leads to reduction in both mRNA and protein levels of IFN-gamma. Overexpression of PPAR-gamma in PPAR-gamma-null NK cells reduces IFN-gamma gene expression. However, PPAR-gamma expression and activation has no effect on NK cell cytolytic activity. In addition, 15d-PGJ(2) but not ciglitazone reduces expression of CD69 in human NK cells, whereas CD44 expression is not affected. These results reveal novel pathways regulating NK cell biologic functions and provide a basis for the design of therapeutic agents that can regulate the function of NK cells within the innate immune response. | lld:pubmed |
| pubmed-article:15265789 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15265789 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15265789 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15265789 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:15265789 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:HodgeDeborah... | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:YoungHoward... | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:ShimozatoOsam... | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:OrtaldoJohn... | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:ReynoldsDella... | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:ZhangXiaX | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:Rodriguez-Gal... | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:WangJi-MingJM | lld:pubmed |
| pubmed-article:15265789 | pubmed:author | pubmed-author:SubleskiJeff... | lld:pubmed |
| pubmed-article:15265789 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15265789 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:15265789 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:15265789 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15265789 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15265789 | pubmed:pagination | 3276-84 | lld:pubmed |
| pubmed-article:15265789 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:meshHeading | pubmed-meshheading:15265789... | lld:pubmed |
| pubmed-article:15265789 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15265789 | pubmed:articleTitle | Peroxisome proliferator-activated receptor-gamma and its ligands attenuate biologic functions of human natural killer cells. | lld:pubmed |
| pubmed-article:15265789 | pubmed:affiliation | Laboratory of Experimental Immunology, Center for Cancer Reseach, National Cancer Institute-Frederick, National Institutes of Health, Frederick, MD 21702-1201, USA. | lld:pubmed |
| pubmed-article:15265789 | pubmed:publicationType | Journal Article | lld:pubmed |
| entrez-gene:5468 | entrezgene:pubmed | pubmed-article:15265789 | lld:entrezgene |
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