Linked Life Data

9461440

Source:http://linkedlifedata.com/resource/pubmed/id/9461440

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5353
pubmed:dateCreated
1998-3-5
pubmed:abstractText
The generation of autoantibody and subsequent tissue deposition of immune complexes (IC) is thought to trigger the pathogenic consequences of systemic autoimmune disease. Modulation of the autoantibody response disrupts pathogenesis by preventing the formation of ICs; however, uncoupling IC formation from subsequent inflammatory responses seems unlikely because of the apparent complexity of the IC-triggered inflammatory cascade. However, the disruption of a single gene, which encodes the gamma chain of the Fc receptor, was found to achieve this uncoupling in a spontaneous model of lupus nephritis, the New Zealand Black/New Zealand White (NZB/NZW) mouse. Gamma chain-deficient NZB/NZW mice generated and deposited IC and activated complement, but were protected from severe nephritis, thus defining another potential pathway for therapeutic intervention in autoimmune disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1052-4
pubmed:dateRevised
2007-3-19
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Uncoupling of immune complex formation and kidney damage in autoimmune glomerulonephritis.
pubmed:affiliation
Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10021, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.