Strain distribution pattern of immune nephritis--a follow-up study
Author(s) -
Chun Xie,
Ziaur S. M. Rahman,
Shuang Xie,
Jili Zhu,
Yong Du,
Xiaohong Qin,
Hui Zhou,
Xin Zhou,
Chandra Mohan
Publication year - 2008
Publication title -
international immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.86
H-Index - 134
eISSN - 1460-2377
pISSN - 0953-8178
DOI - 10.1093/intimm/dxn030
Subject(s) - nephritis , immune system , glomerulonephritis , immunology , azotemia , inbred strain , strain (injury) , proteinuria , biology , kidney , gene , genetics , endocrinology , renal function , anatomy
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.
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