In:
The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 49.19-49.19
Abstract:
Laboratory strains of mice differ in their susceptibility to immune-mediated nephritis. Whereas NZW, DBA1 and 129/svJ strains of mice are highly susceptible to anti-GBM induced nephritis, most other laboratory strains, including C57BL/6 and BALB/c have significantly less disease. In order to uncover susceptibility genes for immune-mediated nephritis, a panel of 156 (129 x BALB/c)F2 mice were bred, challenged with anti-GBM antibodies and phenotyped for nephritis. About 40% of these F2 progeny had evidence of severe nephritis. Genotyping and linkage analysis revealed 2 strongly recessive 129/svJ loci for glomerulonephritis, one on chromosome 2 (linked to rs6295520, P=0.0008) and the second on chromosome 14 (linked to rs3701623, P=0.0004). Proteinuria was strongly linked to 3 recessive 129/svJ loci, including rs3677657 on chr. 7 (P=0.0026), rs3711424 on chr. 13 (P=0.0001), and the chromosome 14 locus for GN. Among these, the loci on Chr 7 and 14 were also strongly linked to glomerular crescent formation, operating additively. To summarize, recessive loci on chromosomes 2, 7, 13 and 14 account for the enhanced susceptibility to nephritis in 129/svJ mice. Congenic dissection studies and candidate gene testing are in progress.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.182.Supp.49.19
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2009
detail.hit.zdb_id:
1475085-5
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