Strain distribution pattern of immune nephritis - A follow-up study

Chun Xie; Ziaur S M Rahman; Shangkui Xie; Jiankun Zhu; Yong Du; Xiangmei Qin; Hui Zhou; Xin J. Zhou; Chandra Mohan

doi:10.1093/intimm/dxn030

Strain distribution pattern of immune nephritis - A follow-up study

Chun Xie, Ziaur S M Rahman, Shangkui Xie, Jiankun Zhu, Yong Du, Xiangmei Qin, Hui Zhou, Xin J. Zhou, Chandra Mohan

Internal Medicine

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	719-728
Number of pages	10
Journal	International Immunology
Volume	20
Issue number	6
DOIs	https://doi.org/10.1093/intimm/dxn030
State	Published - Jun 2008

Keywords

Antibodies
Autoimmunity
C58
Inflammation
Mouse models

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1093/intimm/dxn030

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title = "Strain distribution pattern of immune nephritis - A follow-up study",

abstract = "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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author = "Chun Xie and Rahman, {Ziaur S M} and Shangkui Xie and Jiankun Zhu and Yong Du and Xiangmei Qin and Hui Zhou and Zhou, {Xin J.} and Chandra Mohan",

year = "2008",

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doi = "10.1093/intimm/dxn030",

language = "English (US)",

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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.

KW - Antibodies

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KW - Inflammation

KW - Mouse models

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Strain distribution pattern of immune nephritis - A follow-up study

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Keywords

ASJC Scopus subject areas

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