Source:http://linkedlifedata.com/resource/pubmed/id/11129658
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rdf:type | |
lifeskim:mentions |
umls-concept:C0021311,
umls-concept:C0024426,
umls-concept:C0024432,
umls-concept:C0026912,
umls-concept:C0028128,
umls-concept:C0030685,
umls-concept:C0035820,
umls-concept:C0123759,
umls-concept:C0178719,
umls-concept:C0205263,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1456820,
umls-concept:C1963578
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pubmed:issue |
6
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pubmed:dateCreated |
2000-12-20
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pubmed:abstractText |
IL-12 is believed to play an important role in cell-mediated immunity against intracellular infection primarily by acting on T and NK cells. Recent evidence has suggested, however, that IL-12 has broader cellular targets than previously thought. In this study, we examined the role of IL-12 in macrophage TNF-alpha and nitric oxide (NO) release by using an in vitro model of intracellular infection. IL-12 alone released relatively little TNF-alpha and NO, whereas live mycobacteria alone released TNF-alpha markedly but little NO from murine alveolar macrophages. However, IL-12 and mycobacteria together enhanced TNF-alpha and NO release synergistically. Because IL-12 and mycobacteria also released IFN-gamma from macrophages synergistically, and exogenous IFN-gamma with mycobacteria enhanced TNF-alpha and NO release synergistically, we examined the role of endogenous IFN-gamma in IL-12/mycobacteria-stimulated macrophage activation. Using macrophages from mice deficient in IFN-gamma, we found that IL-12/mycobacteria-enhanced macrophage TNF-alpha and NO release was mediated through endogenous IFN-gamma. We further demonstrated that IFN-gamma and mycobacteria together had a selective effect on macrophage cytokine release because they released TNF-alpha synergistically but not macrophage chemotactic protein-1 (MCP-1). These findings reveal that IL-12 can activate macrophages potently during intracellular infection, and this activating effect is mediated primarily through its effect on macrophage IFN-gamma release.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0741-5400
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
897-902
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11129658-Animals,
pubmed-meshheading:11129658-Female,
pubmed-meshheading:11129658-Gene Expression Regulation,
pubmed-meshheading:11129658-Interferon-gamma,
pubmed-meshheading:11129658-Interleukin-12,
pubmed-meshheading:11129658-Macrophage Activation,
pubmed-meshheading:11129658-Macrophages, Alveolar,
pubmed-meshheading:11129658-Male,
pubmed-meshheading:11129658-Mice,
pubmed-meshheading:11129658-Mice, Inbred C57BL,
pubmed-meshheading:11129658-Mice, Knockout,
pubmed-meshheading:11129658-Mycobacterium bovis,
pubmed-meshheading:11129658-Nitric Oxide,
pubmed-meshheading:11129658-Recombinant Proteins,
pubmed-meshheading:11129658-Tumor Necrosis Factor-alpha
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pubmed:year |
2000
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pubmed:articleTitle |
Role of IL-12 in macrophage activation during intracellular infection: IL-12 and mycobacteria synergistically release TNF-alpha and nitric oxide from macrophages via IFN-gamma induction.
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pubmed:affiliation |
Department of Pathology and Molecular Medicine, Centre for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada. xingz@fhs.mcmaster.ca
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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