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Localization of fluorescein-labeled antinucleoside antibodies in glomeruli of patients with active systemic lupus erythematosus nephritis

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TLDR
The findings are consistent with the hypothesis that antigen-antibody complexes, formed by denatured DNA, specific antibody, and complement, are present in the deposits of foreign material accumulated in the GCW of patients with active SLE glomerulonephritis, and that they may contribute to the pathogenesis of this renal disease.
Abstract
Renal tissues from two groups of patients were studied with fluorescein-labeled (Fl-) antibodies (Abs) to immunoglobulins, complement, and antibodies prepared in rabbits against BSA conjugate of 5-methyluridine (T) and cytidine (C), the latter two of which react specifically with denatured DNA. The first group consisted of 13 SLE patients, and the second consisted of 53 patients with non-SLE nephropathies. The data obtained from the two groups of patients were used for comparison, and they showed the following:(a) Fl-Abs to immunoglobulins and complement were bound in the glomeruli of tissues from all patients with active SLE glomerulonephritis characterized by deposits of foreign material in glomerular capillary walls (GCW). The fluorescent pattern was granular, corresponding to the distribution of the glomerular deposits, as seen by electron microscopy. Fl-Abs reactive with thymine and cytosine were bound in the GCW of eight of the nine patients with active SLE glomerulonephritis and showed the same granular distribution. The capacity of these latter Fl-Abs to stain the GCW was removed by absorption with the homologous antigen or denatured DNA.(b) Fl-Abs to immunoglobulins, complement, and pyrimidine bases of DNA did not react with the GCW of two SLE patients without clinical and histologic evidence of glomerulonephritis or with the sclerotic glomeruli of two uremic patients with chronic "burned out" lupus nephritis.(c) The glomeruli of 47 of the 53 patients with other nephropathies bound Fl-Abs to immunoglobulins and complement to some extent, and in 26, the localization appeared as marked as in the patients with active SLE glomerulonephritis. Fl-Abs reactive with thymine and cytosine were bound in the GCW of only one of the renal tissues from the 53 non-SLE patients. In the remaining 52, no binding was seen.(d) The findings are consistent with the hypothesis that antigen-antibody complexes, formed by denatured DNA, specific antibody, and complement, are present in the deposits of foreign material accumulated in the GCW of patients with active SLE glomerulonephritis, and that they may contribute to the pathogenesis of this renal disease.

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Journal ArticleDOI

Restricted subpopulations of DNA antibodies in kidneys of mice with systemic lupus. Comparison of antibodies in serum and renal eluates.

TL;DR: Sera from MRL/1, BXSB, and NZB/NZW mice, which develop IgG antibodies to DNA and glomerular deposits of DNA-antiDNA immune complexes, were studied by isoelectric focusing, finding that anti-DNA with isOElectric points from pH 8.0--9.0 may be more pathogenic for the kidney than other subpopulations.
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The occurrence of single-stranded DNA in the serum of patients with systemic lupus erythematosus and other diseases.

TL;DR: Single-stranded DNA (SDNA) occurs in high incidence and in greatest concentration in the sera of patients with systemic lupus erythematosus and in several other diseases in which a low incidence of anti-SDNA antibodies is observed.
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Recombinant human Dnase I (rhDNase) in patients with lupus nephritis.

TL;DR: RhDNase was well tolerated without significant adverse events following administration, and treatment was not associated with the development of neutralizing antibodies to rhDNase, and markers of disease activity were unchanged during the study period.
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Procainamide-induced lupus erythematosus. Clinical and laboratory observations

TL;DR: Patients with procainamide-induced lupus appear to have anti-body to denatured DNA and nucleohistone, but in contrast to idiopathic SLE, have little or no antibody to native DNA.
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Antibodies to intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 prevent crescent formation in rat autoimmune glomerulonephritis.

TL;DR: The administration of monoclonal antibodies to rat ICAM-1 and LFA-1 markedly decreased the severity of the renal disease and progression of the disease was appreciably retarded, and the decrease in renal function was inhibited.
References
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Journal ArticleDOI

Immunological studies concerning the nephritis of systemic lupus erythematosus

TL;DR: The immunochemical evidence for the high specific activity of antinuclear antibodies and the association of DNA antigen with DNA antibody in glomeruli add further support for the antigen-antibody complex hypothesis for renal injury in systemic lupus erythematosus.
Journal ArticleDOI

Antibodies specific for ribonucleosides and ribonucleotides and their reaction with dna.

TL;DR: These findings show that the major component of bacteriochlorophyll is inert with respect to the foregoing light-induced activities, and that a special kind of reaction center is needed for the photochemistry that leads to photosynthesis.
Journal ArticleDOI

Complement Fixation with Cell Nuclei and DNA in Lupus Erythematosus

TL;DR: Sera from patients with active lupus erythematosus fixed complement with a wide variety of nuclei from different organs and species, with calf thymus nucleoprotein, and in two instances with histone, suggesting the presence of 2 distinct serum factors.
Journal ArticleDOI

An electron microscope study of the glomerulus in nephrosis, glomerulonephritis, and lupus erythematosus

TL;DR: Renal biopsies from 16 patients with nephrosis, 7 patients with glomerulonephritis, and 3 patients with disseminated lupus erythematosus were studied with the electron microscope to indicate that early in the course of each of these diseases alterations occur in the fine structure of the glomeruli which serve to distinguish one disease process from another.
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