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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2009-8-19
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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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Fungal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD1d,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interferon,
http://linkedlifedata.com/resource/pubmed/chemical/interferon gamma receptor
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1521-4141
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pubmed:author |
pubmed-author:D JordöEmilieE,
pubmed-author:JohanssonCatharinaC,
pubmed-author:KarlssonMaria AMA,
pubmed-author:KarlssonMikael C IMC,
pubmed-author:KuylenstiernaCarlottaC,
pubmed-author:LindSara MSM,
pubmed-author:LundebergLenaL,
pubmed-author:MollMarkusM,
pubmed-author:SandbergJohan KJK,
pubmed-author:ScheyniusAnnikaA,
pubmed-author:T LinderMariaM,
pubmed-author:WinqvistOlaO
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pubmed:issnType |
Electronic
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2293-301
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pubmed:meshHeading |
pubmed-meshheading:19637196-Adolescent,
pubmed-meshheading:19637196-Adult,
pubmed-meshheading:19637196-Aged,
pubmed-meshheading:19637196-Animals,
pubmed-meshheading:19637196-Antibodies, Fungal,
pubmed-meshheading:19637196-Antigens, CD1d,
pubmed-meshheading:19637196-Cell Line,
pubmed-meshheading:19637196-Cells, Cultured,
pubmed-meshheading:19637196-Dermatitis, Atopic,
pubmed-meshheading:19637196-Female,
pubmed-meshheading:19637196-Humans,
pubmed-meshheading:19637196-Immunoglobulin E,
pubmed-meshheading:19637196-Interferon-gamma,
pubmed-meshheading:19637196-Interleukin-18,
pubmed-meshheading:19637196-Malassezia,
pubmed-meshheading:19637196-Male,
pubmed-meshheading:19637196-Mice,
pubmed-meshheading:19637196-Mice, Inbred C57BL,
pubmed-meshheading:19637196-Mice, Knockout,
pubmed-meshheading:19637196-Middle Aged,
pubmed-meshheading:19637196-NF-kappa B,
pubmed-meshheading:19637196-Natural Killer T-Cells,
pubmed-meshheading:19637196-Receptors, Interferon,
pubmed-meshheading:19637196-Signal Transduction,
pubmed-meshheading:19637196-Young Adult
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pubmed:year |
2009
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pubmed:articleTitle |
IL-18 skews the invariant NKT-cell population via autoreactive activation in atopic eczema.
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pubmed:affiliation |
Clinical Allergy Research Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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