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International Immunology Advance Access published online on April 1, 2008
International Immunology, doi:10.1093/intimm/dxn030
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Strain distribution pattern of immune nephritis—a follow-up study

Chun Xie1, Ziaur S. M. Rahman2, Shangkui Xie1, Jiankun Zhu1, Yong Du1, Xiangmei Qin1, Hui Zhou3, Xin J. Zhou3,* and Chandra Mohan1,*

1 Division of Rheumatology, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA
2 Department of Microbiology and Immunology and Kimmel Cancer Center, Jefferson Medical College, Philadelphia, PA 19107, USA
3 Department of Pathology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA

Correspondence to: Correspondence to: C. Mohan; E-mail: chandra.mohan{at}utsouthwestern.edu

Previous studies have indicated that the NZW, DBA/1, 129/sv and BUB strains are particularly sensitive to experimental anti-glomerular basement membrane (GBM)-induced immune nephritis. The present study extends previous observations by examining eight additional inbred mouse strains for their susceptibility to immune nephritis. Unlike the ALR/Lt, CAST/Ei, DDY/JclSidSeyFrk, FVB/NJ, PERA/Ei, SB/Le and BALB/c strains, the C58 mouse strain was observed to be particularly susceptible to experimental immune nephritis, with CBA mice being a close second. In contrast to the other strains, C58 mice uniformly developed heavy proteinuria, azotemia and severe glomerulonephritis with prominent crescent formation and tubulointerstitial nephritis following challenge with anti-GBM sera. These differences were associated with increased murine Ig deposition, leukocyte infiltration and IFN-{gamma} production within the kidneys of C58 mice. Studies aimed at elucidating the genetic factors and molecular pathways responsible for the enhanced renal disease in C58 mice are warranted.

Keywords: antibodies, autoimmunity, C58, inflammation, mouse models

* These authors are co-senior authors.

Transmitting editor: S. Izui

Received 7 December 2006, accepted 24 February 2008.


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