Proteinuria of Nonautoimmune Origin in Wild-type FVB/NJ Mice

FVB/NJ mice frequently are used as transgenic hosts, but the suitability of this genetic background for transgenic and congenic models of systemic autoimmunity have not been reported. In this study, FVB/NJ mice were evaluated for the presence of serum autoantibodies and autoimmune kidney pathology....

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Bibliographic Details
Published in:Comparative medicine 2007-06, Vol.57 (3), p.255-266
Main Authors: Maier, Shannon M, Gross, Joanne K, Hamlin, Kassie L, Maier, Julie L, Workman, Jennifer L, Kim-Howard, Xana R, Schoeb, Trenton R, Farris, A Darise
Format: Article
Language:English
Subjects:
Albuminuria - metabolism
Animals
Antibodies, Antinuclear - blood
Autoimmunity - physiology
Cholesterol - blood
Creatinine - urine
Disease Models, Animal
Female
Fluorescent Antibody Technique
Glomerular Basement Membrane - metabolism
Glomerular Basement Membrane - ultrastructure
Immunoglobulin G - metabolism
Kidney - metabolism
Kidney - pathology
Kidney - ultrastructure
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Microscopy, Electron, Transmission
Nephrosis, Lipoid - immunology
Podocytes - ultrastructure
Specific Pathogen-Free Organisms
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Summary:FVB/NJ mice frequently are used as transgenic hosts, but the suitability of this genetic background for transgenic and congenic models of systemic autoimmunity have not been reported. In this study, FVB/NJ mice were evaluated for the presence of serum autoantibodies and autoimmune kidney pathology. Previously unreported albuminuria was observed in aged female FVB/NJ mice; however, serum autoantibody testing, light microscopic evaluation of differentially stained renal sections, and evaluation of renal sections for immunoglobulin deposits revealed that the albuminuria was not of autoimmune etiology. Anecdotally, multiple characteristics of the FVB/NJ strain, including albuminuria, cholesterolemia, mild podocyte foot process effacement in aged female FVB/NJ kidneys and predisposition to enhanced Th2 immune responses, is reminiscent of human minimal change nephrotic syndrome (MCNS). We propose that mapping of genetic polymorphisms that are responsible for these traits in FVB/NJ mice may lead to increased understanding of mild nephrotic syndromes including MCNS and other proteinurias.
ISSN:1532-0820