TY - JOUR
T1 - Strain distribution pattern of immune nephritis - A follow-up study
AU - Xie, Chun
AU - Rahman, Ziaur S.M.
AU - Xie, Shangkui
AU - Zhu, Jiankun
AU - Du, Yong
AU - Qin, Xiangmei
AU - Zhou, Hui
AU - Zhou, Xin J.
AU - Mohan, Chandra
PY - 2008/6
Y1 - 2008/6
N2 - 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-γ 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.
AB - 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-γ 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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U2 - 10.1093/intimm/dxn030
DO - 10.1093/intimm/dxn030
M3 - Article
C2 - 18381352
AN - SCOPUS:44849093863
SN - 0953-8178
VL - 20
SP - 719
EP - 728
JO - International immunology
JF - International immunology
IS - 6
ER -