Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-9-9
pubmed:abstractText
It is postulated that IFN-gamma confers susceptibility to immunologically mediated tissue injury. To test this hypothesis, we compared the intensity of accelerated anti-glomerular basement membrane glomerulonephritis between wild-type (IFN-gamma+/+) and IFN-gamma gene knockout (IFN-gamma-/-) mice. This disease model is initiated by binding of heterologous (sheep) anti-glomerular basement membrane Abs to the glomeruli of mice preimmunized with sheep IgG. The secondary cellular and humoral immune responses to the planted Ag then lead to albuminuria and glomerular pathology. We found that IFN-gamma-/- mice or IFN-gamma+/+ mice injected with IFN-gamma-neutralizing Ab develop worse albuminuria and glomerular pathology than IFN-gamma+/+ mice. The humoral response to sheep IgG (serum mouse anti-sheep IgG titers and intraglomerular mouse IgG deposits) was comparable in the IFN-gamma+/+ and IFN-gamma-/- groups. In contrast, IFN-gamma-/- mice mounted a stronger cellular immune response (cutaneous delayed-type hypersensitivity reaction) to sheep IgG than IFN-gamma+/+ mice. These findings provide evidence that endogenous IFN-gamma has a protective role in immunologically mediated glomerulonephritis initiated by foreign Ags.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2243-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10438967-Albuminuria, pubmed-meshheading:10438967-Animals, pubmed-meshheading:10438967-Anti-Glomerular Basement Membrane Disease, pubmed-meshheading:10438967-Antibodies, Anti-Idiotypic, pubmed-meshheading:10438967-Basement Membrane, pubmed-meshheading:10438967-Binding Sites, Antibody, pubmed-meshheading:10438967-Cell Movement, pubmed-meshheading:10438967-Disease Susceptibility, pubmed-meshheading:10438967-Hypersensitivity, Delayed, pubmed-meshheading:10438967-Immunoglobulin G, pubmed-meshheading:10438967-Interferon-gamma, pubmed-meshheading:10438967-Kidney Glomerulus, pubmed-meshheading:10438967-Macrophages, pubmed-meshheading:10438967-Male, pubmed-meshheading:10438967-Mice, pubmed-meshheading:10438967-Mice, Inbred C57BL, pubmed-meshheading:10438967-Mice, Knockout, pubmed-meshheading:10438967-Monocytes, pubmed-meshheading:10438967-Neutrophils, pubmed-meshheading:10438967-Nitrates, pubmed-meshheading:10438967-Nitrites
pubmed:year
1999
pubmed:articleTitle
Increased susceptibility to immunologically mediated glomerulonephritis in IFN-gamma-deficient mice.
pubmed:affiliation
Medical and Research Services, Veterans Affairs Medical Center, Renal Division, Department of Medicine, Emory University, Atlanta, GA 30033, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't