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From the Carcinogenesis Program, Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830
Abstract
Naturally occurring glomerulonephritis in conventional NZB (1), AKR (2), and RF (3) mice has been associated with an immune complex etiology. In all three cases, it has been demonstrated that the glomerular lesion is a result, in part, of chronic deposition of immune complexes of endogenous Gross virus-specific cell surface and/or soluble antigens with "G natural" antibody. Glomerular lesions of this type also have been observed in AKR (4) and BALB/c (5) mice with experimentally induced leukemias, and in the latter study they were specifically associated with immune complexes involving antigens of the exogenous murine leukemia virus (MuLV).3 At the ultrastructural level, this glomerulonephritis is characterized by marked thickening of localized regions of the glomerular basement membrane (5, 6), which is thought to result from the immune complex deposition (7). We report here the localization of intact endogenous C-type virus within the basement membrane of aged AKR mice showing evidence of chronic glomerulonephritis.
Footnotes
1 This work was supported jointly by the National Cancer Institute and the United States Atomic Energy Commission under contract with the Union Carbide Corp.
3 Abbreviations used in this paper: MuLV, murine leukemia virus; IF, immunofluorescence; gs-1, groupspecific 1 antigen.
2 Postdoctoral investigator of the University of TennesseeOak Ridge Graduate School of Biomedical Sciences.
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