Source:http://linkedlifedata.com/resource/pubmed/id/11937527
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2002-4-8
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pubmed:abstractText |
Dendritic cell (DC)-dependent activation of liver NKT cells triggered by a single i.v. injection of a low dose (10-100 ng/mouse) of alpha-galactosyl ceramide (alphaGalCer) into mice induces liver injury. This response is particularly evident in HBs-tg B6 mice that express a transgene-encoded hepatitis B surface Ag in the liver. Liver injury following alphaGalCer injection is suppressed in mice depleted of NK cells, indicating that NK cells play a role in NK T cell-initiated liver injury. In vitro, liver NKT cells provide a CD80/86-dependent signal to alphaGalCer-pulsed liver DC to release IL-12 p70 that stimulates the IFN-gamma response of NKT and NK cells. Adoptive transfer of NKT cell-activated liver DC into the liver of nontreated, normal (immunocompetent), or immunodeficient (RAG(-/-) or HBs-tg/RAG(-/-)) hosts via the portal vein elicited IFN-gamma responses of liver NK cells in situ. IFN-beta down-regulates the pathogenic IL-12/IFN-gamma cytokine cascade triggered by NKT cell/DC/NK cell interactions in the liver. Pretreating liver DC in vitro with IFN-beta suppressed their IL-12 (but not IL-10) release in response to CD40 ligation or specific (alphaGalCer-dependent) interaction with liver NKT cells and down-regulated the IFN-gamma response of the specifically activated liver NKT cells. In vivo, IFN-beta attenuated the NKT cell-triggered induction of liver immunopathology. This study identifies interacting subsets of the hepatic innate immune system (and cytokines that up- and down-regulate these interactions) activated early in immune-mediated liver pathology.
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Galactosylceramides,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins
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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 |
15
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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 |
3763-70
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11937527-Adoptive Transfer,
pubmed-meshheading:11937527-Animals,
pubmed-meshheading:11937527-Antigens, CD,
pubmed-meshheading:11937527-Antigens, CD80,
pubmed-meshheading:11937527-Antigens, CD86,
pubmed-meshheading:11937527-Cells, Cultured,
pubmed-meshheading:11937527-Coculture Techniques,
pubmed-meshheading:11937527-Cytotoxicity, Immunologic,
pubmed-meshheading:11937527-Dendritic Cells,
pubmed-meshheading:11937527-Galactosylceramides,
pubmed-meshheading:11937527-Immunosuppressive Agents,
pubmed-meshheading:11937527-Injections, Intravenous,
pubmed-meshheading:11937527-Interferon-beta,
pubmed-meshheading:11937527-Interleukin-12,
pubmed-meshheading:11937527-Killer Cells, Natural,
pubmed-meshheading:11937527-Liver,
pubmed-meshheading:11937527-Lymphocyte Activation,
pubmed-meshheading:11937527-Membrane Glycoproteins,
pubmed-meshheading:11937527-Mice,
pubmed-meshheading:11937527-Mice, Inbred C57BL,
pubmed-meshheading:11937527-Mice, Knockout,
pubmed-meshheading:11937527-Mice, Transgenic,
pubmed-meshheading:11937527-T-Lymphocyte Subsets
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pubmed:year |
2002
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pubmed:articleTitle |
Activating immunity in the liver. II. IFN-beta attenuates NK cell-dependent liver injury triggered by liver NKT cell activation.
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pubmed:affiliation |
Department of Physiology and Immunology, Medical Faculty, University of Rijeka, Rijeka, Croatia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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