| http://purl.uniprot.org/citations/12819238 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12819238 | http://www.w3.org/2000/01/rdf-schema#comment | "Macrophages are prominent participants in crescentic glomerulonephritis (GN) and have been suggested to be the major source of TNF in this cell-mediated form of glomerular inflammation. Intrinsic renal cells also have the capacity to produce TNF. For dissecting the contribution of local versus bone marrow (BM)-derived TNF in inflammatory renal injury, TNF chimeric mice were created by transplanting normal wild-type (WT) BM into irradiated TNF-deficient recipients (WT-->TNF-/- chimeras) and vice versa (TNF-/--->WT chimeras). A model of crescentic GN induced by an intravenous injection of sheep anti-murine glomerular basement membrane antibody was studied in WT mice, mice with complete TNF deficiency (TNF-/-), and chimeric mice. Crescentic GN was attenuated in TNF-/- mice with fewer crescents (crescents, 13.7 +/-1.7% of glomeruli) and reduced functional indices of renal injury (serum creatinine, 15.2 +/- 0.8 micromol/L). Similar protection (crescents, 14.3 +/-1.9% of glomeruli; serum creatinine, 18.9 +/-1.1 micromol/L) was observed in chimeric mice with intact BM but absent renal-derived TNF (WT-->TNF-/-chimeras), suggesting a minor contribution of infiltrating leukocytes to TNF-mediated renal injury. Chimeric mice with TNF-deficient leukocytes but intact intrinsic renal cell-derived TNF (crescents, 20.5 +/-2.0% of glomeruli; serum creatinine, 21.6 +/-1.4 micromol/L) developed similar crescentic GN to WT mice (crescents, 22.3 +/-1.4% of glomeruli; serum creatinine, 24.8 +/-1.9 micromol/L). Cutaneous delayed-type hypersensitivity after subdermal challenge with the nephritogenic antigen was attenuated in the absence of BM cell-derived TNF but unaffected in WT-->TNF-/-chimeric mice. These studies suggest that intrinsic renal cells are the major cellular source of TNF contributing to inflammatory injury in crescentic GN."xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.org/dc/terms/identifier | "doi:10.1097/01.asn.0000073902.38428.33"xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/author | "Holdsworth S.R."xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/author | "Sedgwick J.D."xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/author | "Tipping P.G."xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/author | "Timoshanko J.R."xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/name | "J Am Soc Nephrol"xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/pages | "1785-1793"xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/title | "Intrinsic renal cells are the major source of tumor necrosis factor contributing to renal injury in murine crescentic glomerulonephritis."xsd:string |
| http://purl.uniprot.org/citations/12819238 | http://purl.uniprot.org/core/volume | "14"xsd:string |
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