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arthus reaction/proteinuria
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6 risultati
Fc receptor-independent development of autoimmune glomerulonephritis in lupus-prone MRL/lpr mice.
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OBJECTIVE
To determine the role of Fc receptors (FcR), which play crucial roles in antibody and immune complex-mediated inflammation and autoimmunity, including glomerulonephritis (GN), in the development of autoimmune GN and vasculitis in MRL/lpr mice, one of the most widely used lupus-prone mouse
[Immune tolerance in Masugi nephritis].
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Induction of immunotolerance was studied in the autologous phase of experimental rabbit glomerulonephritis. The glomerulonephritis was induced by intravenous injection of duck anti-rabbit glomerular basement membrane globulin into rabbits. One single intravenous injection of that nephrotoxis
Treatment of lupus-prone NZB/NZW F1 mice with recombinant soluble Fc gamma receptor II (CD32).
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OBJECTIVE
Systemic lupus erythematosus (SLE) is a classical autoimmune disorder characterised by the production of IgG autoantibodies against double-stranded DNA (dsDNA). Activation of Fc gamma R-bearing effector cells by immune complexes (ICs) is a key event in SLE pathogenesis as lupus-prone
[The effect of cyclosporin A on experimental glomerulonephritis in rabbits].
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The effect of cyclosporin A on the development of the autologous phase of experimental rabbit glomerulonephritis was assessed. The glomerulonephritis was induced by an intravenous injection of duck anti-rabbit glomerular basement membrane globulin into adult rabbits. After 5-7 days, diffuse
The effect of cyclosporin A on rabbit nephrotoxic glomerulonephritis.
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The effect of cyclosporin A on the development of the autologous phase of experimental rabbit glomerulonephritis was assessed. The glomerulonephritis was induced by a single intravenous injection of duck anti-rabbit glomerular basement membrane globulin (molecular weight: 115 kDa) into adult
The localization of circulating immune complexes in experimental serum sickness. The role of vasoactive amines and hydrodynamic forces.
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In serum sickness, mechanisms by which circulating immune complexes become localized in the walls of vessels and glomeruli have been studied. In affected arteries, morphologic observations showed that circulating marker particles of carbon would rapidly deposit along the luminal surface of the
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