Abstract |
Lupus nephritis is an immune-mediated disease, where antibodies and T cells both play pathogenic roles. Since spontaneous lupus nephritis in mouse models takes 6-12 months to manifest, there is an urgent need for a mouse model that can be used to delineate the pathogenic processes that lead to immune nephritis, over a quicker time frame. We propose that the experimental anti-glomerular basement membrane (GBM) disease model might be a suitable tool for uncovering some of the molecular steps underlying lupus nephritis. This article reviews the current evidence that supports the use of the experimental anti-GBM nephritis model for studying spontaneous lupus nephritis. Importantly, out of about 25 different molecules that have been specifically examined in the experimental anti-GBM model and also spontaneous lupus nephritis, all influence both diseases concordantly, suggesting that the experimental model might be a useful tool for unraveling the molecular basis of spontaneous lupus nephritis. This has important clinical implications, both from the perspective of genetic susceptibility as well as clinical therapeutics.
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Authors | Yuyang Fu, Yong Du, Chandra Mohan |
Journal | Clinical immunology (Orlando, Fla.)
(Clin Immunol)
Vol. 124
Issue 2
Pg. 109-18
(Aug 2007)
ISSN: 1521-6616 [Print] United States |
PMID | 17640604
(Publication Type: Journal Article, Review)
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Topics |
- Animals
- Anti-Glomerular Basement Membrane Disease
(genetics, immunology)
- Disease Models, Animal
- Humans
- Lupus Nephritis
(genetics, immunology)
- Mice
- Rats
- T-Lymphocytes
(immunology)
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