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

被引:51
作者
Fu, Yuyang [1 ]
Du, Yong [1 ]
Mohan, Chandra [1 ]
机构
[1] Univ Texas, SW Med Sch, Dept Internal Med Rheumatol & Immunol, Dallas, TX 75390 USA
关键词
lupus; nephritis; genetics; animal models; inflammation; GLOMERULAR-BASEMENT-MEMBRANE; EXPERIMENTAL AUTOIMMUNE GLOMERULONEPHRITIS; COLONY-STIMULATING FACTOR; NEPHROTOXIC SERUM NEPHRITIS; TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; T-CELL EPITOPE; CRESCENTIC GLOMERULONEPHRITIS; MRL-FAS(LPR) MICE; DEFICIENT MICE;
D O I
10.1016/j.clim.2007.05.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
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. (c) 2007 Published by Elsevier Inc.
引用
收藏
页码:109 / 118
页数:10
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