Pathogenesis of early nephritis in lupus prone mice with a genetic accelerating (lpr) factor.
We investigated the relative roles of B cell activity, circulating immune complexes, complement concentration and kinetics of disappearance and uptake of immune complexes from the circulation in the pathogenesis of early nephritis of MRL/lpr mice. In comparison to data in control (C57BL/6J) mice, B cell activity was enhanced and the concentration of autoantibodies and endogenous immune complexes in plasma were increased, whereas complement (C3) concentration was not significantly different in MRL/lpr mice. The kinetics of disappearance of radiolabeled immune complexes from the circulation were similar in MRL/lpr and control mice, whereas uptake of radiolabeled immune complexes by the liver was decreased in MRL/lpr mice. Features of polyclonal B cell activation and impaired mononuclear phagocyte function are early events that may set the stage for progressive systemic involvement in MRL/lpr mice.
Granholm
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NA
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Ohio 45267-0529.
Cavallo
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T
D000818:Animals; D000936:Antigen-Antibody Complex / Q000097:blood / Q000378:metabolism; D001323:Autoantibodies / Q000097:blood; D001402:B-Lymphocytes / Q000276:immunology; D003165:Complement System Proteins / Q000378:metabolism; D008181:Lupus Nephritis / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009928:Organ Specificity / Q000276:immunology; D010587:Phagocytosis / Q000502:physiology
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D003165:Complement System Proteins