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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1996-5-29
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pubmed:abstractText |
Cross-communication between glomerular cells and infiltrating mononuclear cells plays an important role in the generation of or recovery from glomerular diseases. We found that cultured mesangial cells secrete a factor that inhibits production of proinflammatory cytokines by activated macrophages. Treatment of J774.2 macrophages with conditioned media from rat mesangial cells blunted the transcriptional induction of IL-1 beta, IL-6, and TNF-alpha by LPS. None of the media conditioned by other fibroblastic, epithelial, or endothelial cell lines exhibited the inhibitory effect. Media conditioned by normal rat glomeruli contained a similar inhibitory activity, which was enhanced in an acute model of mesangial proliferative glomerulonephritis. To identify the active component involved, we examined the expression of known macrophage deactivators IL-10, IL-13, and TGF-beta 1 in mesangial cells. Under the basal culture conditions, strong expression of TGF-beta 1 mRNA was observed, whereas expression of neither IL-10 nor IL-13 was detected. Immunoblot analysis and a specific bioassay detected the active form of TGF-beta 1 exclusively in the mesangial cell conditioned media. The inhibitory activity was enhanced by heat treatment, consistent with the known property of TGF-beta. A specific anti-TGF-beta 1 neutralizing Ab abolished the inhibitory effect exerted by the mesangial cell media, and exogenously added TGF-beta1 suppressed macrophage cytokine expression in a dose-dependent manner. These findings demonstrate that mesangial cells and isolated glomeruli secrete a factor which suppresses cytokine expression by activated macrophages, the active entity being identified as TGF-beta 1.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
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 |
156
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2964-71
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8609417-Animals,
pubmed-meshheading:8609417-Cells, Cultured,
pubmed-meshheading:8609417-Culture Media, Conditioned,
pubmed-meshheading:8609417-Cytokines,
pubmed-meshheading:8609417-Dose-Response Relationship, Immunologic,
pubmed-meshheading:8609417-Glomerular Mesangium,
pubmed-meshheading:8609417-Glomerulonephritis,
pubmed-meshheading:8609417-Lipopolysaccharides,
pubmed-meshheading:8609417-Macrophage Activation,
pubmed-meshheading:8609417-Macrophages,
pubmed-meshheading:8609417-Rats,
pubmed-meshheading:8609417-Rats, Inbred F344,
pubmed-meshheading:8609417-Rats, Sprague-Dawley,
pubmed-meshheading:8609417-Transforming Growth Factor beta
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pubmed:year |
1996
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pubmed:articleTitle |
Transforming growth factor-beta 1 is the predominant paracrine inhibitor of macrophage cytokine synthesis produced by glomerular mesangial cells .
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pubmed:affiliation |
Department of Medicine, University College London Medical School, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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