Authors
Kui Liu, Quan-Zhen Li, Angelica M Delgado-Vega, Anna-Karin Abelson, Elena Sánchez, Jennifer A Kelly, Li Li, Yang Liu, Jinchun Zhou, Mei Yan, Qiu Ye, Shenxi Liu, Chun Xie, Xin J Zhou, Sharon A Chung, Bernardo Pons-Estel, Torsten Witte, Enrique De Ramón, Sang-Cheol Bae, Nadia Barizzone, Gian Domenico Sebastiani, Joan T Merrill, Peter K Gregersen, Gary G Gilkeson, Robert P Kimberly, Timothy J Vyse, Il Kim, Sandra D’Alfonso, Javier Martin, John B Harley, Lindsey A Criswell, Edward K Wakeland, Marta E Alarcón-Riquelme, Chandra Mohan, Profile Study Group, Italian Collaborative Group, German Collaborative Group, Spanish Collaborative Group, Argentinian Collaborative Group, SLEGEN Consortium
Publication date
2009/4/1
Journal
The Journal of clinical investigation
Volume
119
Issue
4
Pages
911-923
Publisher
American Society for Clinical Investigation
Description
Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody–induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that may be responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody–induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family, which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less …
Total citations
Scholar articles
K Liu, QZ Li, AM Delgado-Vega, AK Abelson… - The Journal of clinical investigation, 2009