Source:http://linkedlifedata.com/resource/pubmed/id/11907086
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
2002-3-21
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| pubmed:abstractText |
The epidermal Langerhans cells (LC), a member of the dendritic cell family, and the LC-derived cytokine IL-12 play a pivotal role in the initiation of contact hypersensitivity (CHS), a Th1 immune response in the skin. Because IL-18, another LC-derived cytokine, shares functional and biological properties with IL-12, we examined a potential role for IL-18 in CHS initiation. Our studies demonstrated that during the induction phase of murine CHS, IL-18 mRNA was significantly up-regulated in the skin-draining lymph nodes (LN). Migratory hapten-modified LC in LN expressed high levels of IL-18 mRNA and secreted functional IL-18 protein. LN cells produced significant amounts of IFN-gamma following in vitro IL-12 stimulation, which could be partially blocked by anti-IL-18 Ab, suggesting a synergistic role for endogenous IL-18 in IFN-gamma production by LN cells. Because mature IL-18 requires cleavage of immature precursors by caspase-1, we further examined IL-12-induced IFN-gamma production in caspase-1(-/-) LN cells. An impaired IFN-gamma production was seen in caspase-1(-/-) LN cells, which could be restored by addition of exogenous IL-18, supporting a role for caspase-1-cleaved, mature IL-18 in IFN-gamma production. Finally, in vivo studies showed that CHS responses were significantly inhibited in mice treated with neutralizing IL-18 Ab as well as in caspase-1(-/-) mice deficient in mature IL-18, indicating functional relevance for IL-18 in CHS. Taken together, our studies demonstrate that LC-derived IL-18 significantly contributes to CHS initiation.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Haptens,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-18,
http://linkedlifedata.com/resource/pubmed/chemical/Oxazolone,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
168
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3303-8
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:11907086-Administration, Cutaneous,
pubmed-meshheading:11907086-Animals,
pubmed-meshheading:11907086-Caspase 1,
pubmed-meshheading:11907086-Cell Line,
pubmed-meshheading:11907086-Cell Movement,
pubmed-meshheading:11907086-Dermatitis, Contact,
pubmed-meshheading:11907086-Haptens,
pubmed-meshheading:11907086-Immune Sera,
pubmed-meshheading:11907086-Immunization,
pubmed-meshheading:11907086-Injections, Intraperitoneal,
pubmed-meshheading:11907086-Interferon-gamma,
pubmed-meshheading:11907086-Interleukin-12,
pubmed-meshheading:11907086-Interleukin-18,
pubmed-meshheading:11907086-Langerhans Cells,
pubmed-meshheading:11907086-Lymph Nodes,
pubmed-meshheading:11907086-Mice,
pubmed-meshheading:11907086-Mice, Inbred C57BL,
pubmed-meshheading:11907086-Mice, Knockout,
pubmed-meshheading:11907086-Oxazolone,
pubmed-meshheading:11907086-RNA, Messenger,
pubmed-meshheading:11907086-Up-Regulation
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| pubmed:year |
2002
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| pubmed:articleTitle |
Contribution of Langerhans cell-derived IL-18 to contact hypersensitivity.
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| pubmed:affiliation |
Department of Dermatology, Johns Hopkins University, Baltimore, MD 21287, USA.
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| pubmed:publicationType |
Journal Article
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