| pubmed-article:19637196 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19637196 | lifeskim:mentions | umls-concept:C0032659 | lld:lifeskim |
| pubmed-article:19637196 | lifeskim:mentions | umls-concept:C0383327 | lld:lifeskim |
| pubmed-article:19637196 | lifeskim:mentions | umls-concept:C0011615 | lld:lifeskim |
| pubmed-article:19637196 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:19637196 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:19637196 | pubmed:dateCreated | 2009-8-19 | lld:pubmed |
| pubmed-article:19637196 | pubmed:abstractText | Atopic eczema (AE) is a chronic relapsing inflammatory skin disease where the commensal yeast Malassezia can act as a microbial trigger factor. Malassezia activates human DC to produce IL-18, an innate cytokine that is elevated in serum of AE patients; however, the precise role of IL-18 in human AE etiology is unknown. Herein, we investigated the effect of IL-18 on the human invariant NKT (iNKT) cell compartment in AE. We found that IL-18 was a potent activator of human iNKT-cells and promoted a pro-inflammatory CD1d-dependent response, even in the absence of exogenous ligands. Chronic activation via IL-18 on the other hand was inhibitory and skewed the iNKT-cell pool by selectively suppressing CD4(+) iNKT-cells. This was mimicked in AE patients where the proportion of CD4(+) iNKT-cells was reduced in peripheral blood and coincided with elevated plasma levels of IL-18. Furthermore, a reduced CD4(+) iNKT-cell pool was associated with elevated IgE levels in plasma, and the plasma levels of IL-18 correlated with both total IgE and disease severity in the AE patients. Based on these findings, we propose that IL-18-mediated activation and subsequent dysregulation of the CD1d-restricted iNKT-cells plays a role in the pathogenesis of human AE. | lld:pubmed |
| pubmed-article:19637196 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19637196 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19637196 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19637196 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:19637196 | pubmed:issn | 1521-4141 | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:ScheyniusAnni... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:JohanssonCath... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:WinqvistOlaO | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:MollMarkusM | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:SandbergJohan... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:KarlssonMikae... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:LundebergLena... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:Kuylenstierna... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:LindSara MSM | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:KarlssonMaria... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:D... | lld:pubmed |
| pubmed-article:19637196 | pubmed:author | pubmed-author:T... | lld:pubmed |
| pubmed-article:19637196 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19637196 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:19637196 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19637196 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19637196 | pubmed:pagination | 2293-301 | lld:pubmed |
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| pubmed-article:19637196 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19637196 | pubmed:articleTitle | IL-18 skews the invariant NKT-cell population via autoreactive activation in atopic eczema. | lld:pubmed |
| pubmed-article:19637196 | pubmed:affiliation | Clinical Allergy Research Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. | lld:pubmed |
| pubmed-article:19637196 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19637196 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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