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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0009498,
umls-concept:C0009545,
umls-concept:C0030685,
umls-concept:C0086418,
umls-concept:C0127400,
umls-concept:C0205088,
umls-concept:C0205263,
umls-concept:C0391871,
umls-concept:C0449432,
umls-concept:C0680255,
umls-concept:C1179435,
umls-concept:C1283071,
umls-concept:C1363844,
umls-concept:C1512199,
umls-concept:C1524073,
umls-concept:C1548799,
umls-concept:C1705248,
umls-concept:C1963578
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pubmed:issue |
4
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pubmed:dateCreated |
1992-5-28
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pubmed:abstractText |
Exposure of cultured human glomerular mesangial cells (GMC) to normal human serum and an activator of the complement system results in rapid uptake of the terminal complement proteins C5b-9 by the cells. This 'innocent bystander' complement attack, however, does not result in cell killing, but in the stimulation of the GMC to release prostaglandin E (PGE), interleukin 1 (Il-1) and tumor necrosis factor (TNF). Endogenously synthesized Il-1 in turn activates PGE release, indicating that the C5b-9 attack initiates an autocrine feedback stimulation. Together with the fact that C5b-9 is found in many forms of glomerulonephritis, the data point to a role of the terminal complement proteins in the initiation and perpetuation of an inflammatory response.
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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/Complement Membrane Attack Complex,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandins E,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:issn |
0020-5915
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
96
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
331-7
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading | |
pubmed:year |
1991
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pubmed:articleTitle |
Induction of mediator release from human glomerular mesangial cells by the terminal complement components C5b-9.
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pubmed:affiliation |
Institut für Immunologie und Serologie, Universität Heidelberg, BRD.
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pubmed:publicationType |
Journal Article
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