| pubmed-article:16020503 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16020503 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
| pubmed-article:16020503 | lifeskim:mentions | umls-concept:C0383327 | lld:lifeskim |
| pubmed-article:16020503 | lifeskim:mentions | umls-concept:C0024291 | lld:lifeskim |
| pubmed-article:16020503 | lifeskim:mentions | umls-concept:C0205082 | lld:lifeskim |
| pubmed-article:16020503 | lifeskim:mentions | umls-concept:C0175668 | lld:lifeskim |
| pubmed-article:16020503 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16020503 | pubmed:dateCreated | 2005-11-3 | lld:pubmed |
| pubmed-article:16020503 | pubmed:abstractText | Hemophagocytic syndrome (HPS) is characterized by an uncontrolled and poorly understood activation of T-helper 1 (Th-1) lymphocytes and macrophages. We studied 20 patients with HPS secondary to infections, autoimmune disease, lymphoma, or cancer and observed that the concentrations of serum interleukin 18 (IL-18), a strong inducer of Th-1 responses, interferon gamma (IFN-gamma) production, and stimulation of macrophages and natural killer (NK) cells were highly increased in HPS but not in control patients. In contrast, concentrations of its natural inhibitor, the IL-18 binding protein (IL-18BP), were only moderately elevated, resulting in a high level of biologically active free IL-18 in HPS (4.6-fold increase compared with controls; P < .001). Free IL-18 but not IL-12 concentrations significantly correlated with clinical status and the biologic markers of HPS such as anemia (P < .001), hypertriglyceridemia, and hyperferritinemia (P < .01) and also with markers of Th-1 lymphocyte or macrophage activation, such as elevated concentrations of IFN-gamma and soluble IL-2 and tumor necrosis factor alpha (TNF-alpha) receptor concentrations. Despite high IL-18 elevation, in vitro NK-cell cytotoxicity was severely impaired in HPS patients, in part due to NK-cell lymphopenia that was observed in a majority of patients but also secondary to an intrinsic NK-cell functional deficiency. We concluded that a severe IL-18/IL-18BP imbalance results in Th-1 lymphocyte and macrophage activation, which escapes control by NK-cell cytotoxicity and may allow for secondary HPS in patients with underlying diseases. | lld:pubmed |
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| pubmed-article:16020503 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16020503 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16020503 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16020503 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16020503 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:DinarelloChar... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:NovickDaniela... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:RubinsteinMen... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:PaulPascaleP | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:KaplanskiGill... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:MarinValérieV | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:SchleinitzNic... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:MazodierKarin... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:VeitVéronique... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:HarléJean-Rob... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:FarnarierCath... | lld:pubmed |
| pubmed-article:16020503 | pubmed:author | pubmed-author:RobitailStéph... | lld:pubmed |
| pubmed-article:16020503 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16020503 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16020503 | pubmed:volume | 106 | lld:pubmed |
| pubmed-article:16020503 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16020503 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16020503 | pubmed:pagination | 3483-9 | lld:pubmed |
| pubmed-article:16020503 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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