Experimental anti-GBM disease as a tool for studying spontaneous lupus nephritis.

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.

• 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)

Topics

• Animals
• Anti-Glomerular Basement Membrane Disease (genetics, immunology)
• Disease Models, Animal
• Humans
• Lupus Nephritis (genetics, immunology)
• Mice
• Rats
• T-Lymphocytes (immunology)