Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1998-5-4
pubmed:abstractText
(NZB x NZW)F1 female (BW) mice spontaneously develop an autoimmune disease, characterized by the production of autoantibodies (autoAbs) and glomerulonephritis, which can be delayed by neutralizing IFN-gamma Abs and accelerated by IFN-gamma injections. To define the role of IFN-gamma in the pathogenesis of glomerulonephritis, we established a population of BW mice deficient in IFN-gammaR (BWgammaR[-/-]) by repeated crossing; these mice were compared with BWgammaR(+/+) and +/- littermates. Of the BWgammaR(+/+) and +/- mice, 50% showed immune complex glomerulonephritis with heavy proteinuria at 8 mo of age, while only 10% of the BWgammaR(-/-) mice were affected at 14 mo. The serum concentration of anti-dsDNA and anti-histone Abs was dramatically reduced in BWgammaR(-/-) mice. The role of IFN-gamma in promoting class switch to IgG2a and IgG3 could not fully account for the impaired production of anti-dsDNA in BWgammaR(-/-) animals since, IgM and IgG1 levels were also reduced. There was a high incidence of B cell lymphoma in the BWgammaR(-/-) mice, which might be related to the suppression of autoAb production. Thus, the absence of glomerulonephritis in BWgammaR(-/-) mice is likely due to a dramatic yet unexplained effect of the inactivation of IFN-gamma signaling on autoAb production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3713-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9558072-Animals, pubmed-meshheading:9558072-Antibodies, Antinuclear, pubmed-meshheading:9558072-Autoantibodies, pubmed-meshheading:9558072-Base Sequence, pubmed-meshheading:9558072-DNA Primers, pubmed-meshheading:9558072-Disease Models, Animal, pubmed-meshheading:9558072-Female, pubmed-meshheading:9558072-Immunoglobulin G, pubmed-meshheading:9558072-Interferon-gamma, pubmed-meshheading:9558072-Interleukin-4, pubmed-meshheading:9558072-Lupus Nephritis, pubmed-meshheading:9558072-Lymphoma, pubmed-meshheading:9558072-Male, pubmed-meshheading:9558072-Mice, pubmed-meshheading:9558072-Mice, Inbred NZB, pubmed-meshheading:9558072-Mice, Knockout, pubmed-meshheading:9558072-Polymerase Chain Reaction, pubmed-meshheading:9558072-Receptors, Interferon, pubmed-meshheading:9558072-T-Lymphocytes
pubmed:year
1998
pubmed:articleTitle
IFN-gamma receptor deletion prevents autoantibody production and glomerulonephritis in lupus-prone (NZB x NZW)F1 mice.
pubmed:affiliation
Institute of Anatomy of the University of Zürich, Switzerland.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't