Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2002-10-18
pubmed:abstractText
The complement system is indispensable for host defence. Unregulated activation, however, is related to various diseases. In order to elucidate the significance of complement, methodology that disrupts the complement system is essential. Advances in molecular genetics made direct modulations of the genes of complement components and their regulatory proteins feasible. One method is disruption of genes that encode complement components. Several studies have been conducted with these mice in models such as nephrotoxic serum (NTS) nephritis, ischaemia reperfusion and immune complex-mediated glomerulonephritis. These studies all showed that depletion of complement components ameliorated the severity of the diseases. Complement regulatory protein serves a regulatory role in the complement system. Genetically engineered animals that overexpress these proteins have been employed to elucidate their biological roles. Mice overexpressing soluble complement regulatory proteins were protected from the lesion of both NTS and the glomerular endothelial injury model. In contrast, knockout mice that lack expression of decay-accelerating factor (DAF), a complement regulatory protein, developed severe glomerular lesions when subnephritogenic doses of NTS were administered. These genetically engineered animals shed light on the mechanism of initiation and progression of kidney disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0931-0509
pubmed:author
pubmed:issnType
Print
pubmed:volume
17 Suppl 9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
34-6
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Contribution of genetically engineered animals to the analyses of complement in the pathogenesis of nephritis.
pubmed:affiliation
Division of Nephrology and Endocrinology, University of Tokyo, School of Medicine, Tokyo, Japan.
pubmed:publicationType
Journal Article, Review