Evidence map›Paper›PMID 8252800›Full record

ArticleClinical and experimental immunology1993

Metabolic fate of monovalent and multivalent antibodies of Heymann nephritis following formation of surface immune complexes on glomerular epithelial cells.

A K Singh, B S Kasinath

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Article in Clinical and experimental immunology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

A K SinghDepartment of Medicine, Rush Medical College, Chicago, IL.
B S Kasinath
Loyola University Medical Center · US

Funding

PATHOGENESIS OF GLOMERULAR SUBEPITHELIAL IMMUNE DEPOSITSR01DK035804 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI SINGH, ASHOK K · 1988 to 1992
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GLOMERULAR EPITHELIAL CELLS IN DIABETES MELLITISR01DK041517 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI KASINATH, BALAKUNTALAM S · 1990 to 1994
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CIRCULATORY ANTIGENS IN PATHOGENESIS OF HEYMANN NEPRHRITR23DK035804 · NIDDK · RUSH UNIVERSITY MEDICAL CENTER · PI SINGH, ASHOK K · 1986 to 1987
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NIDDK NIH HHS DK35804NIDDK NIH HHS DK41517
6 · The paper itself

Abstract

Heymann nephritis of the rat has several similarities to human idiopathic membranous glomerulo-nephropathy, and therefore serves as an animal model for study of the human disease. The disease process in the rat is initiated by autoantibodies forming in situ immune deposits on the surface of the glomerular epithelial cell in the lamina rara externa region of the glomerular basement membrane. It is now understood that multispecific antibodies (like anti-gp600) form the nephritogenic deposits which cause proteinuria, while MoAb (like anti-gp330, anti-90 kD and anti-gp70) form only transient deposits which do not give rise to proteinuria. The reasons for differences between pathologic effects of mono- and multispecific antibodies are not known. Following characterization of putative antigens of Heymann nephritis by immunofluorescence, immunogold and immunoblot techniques, we have investigated the metabolic handling of a multispecific (anti-600), monospecific antibody (anti-gp70) and a MoAb (anti-gp330) by the cultured glomerular epithelial cell to gain an insight into the mechanism of nephritogenicity of multispecific antibody. Anti-gp600 reacted to multiple antigens in the 330-kD and 70-kD regions; anti-gp70 reacted to only the 70-kD region. Ultrastructurally, all three types of antigens were present on the plasma membrane, concentrated in the microvillar region. The cells were incubated with the antibodies, and clearance of the antibodies from the cells was evaluated. Following binding, all three antibodies were internalized by the cells. However, it was found that monoclonal anti-gp330 MoAb was cleared most rapidly from the cell (t1/2 5 min), followed by anti-gp70 (t1/2 30 min). Anti-gp600 was cleared at four times slower rate than anti-gp70 (t1/2 2h) by the cell. While anti-gp330 MoAb and monospecific anti-gp70 antibody were expelled from the cell in 25-32% digested form, the multispecific anti-gp600 was digested to the extent of only 5-8%. No immune complexes were detected in the medium with any of the three antibodies. The shed label was in intact IgG form. It is concluded that multispecific antibodies of Heymann nephritis are nephritogenic because of their slower clearance and digestion and therefore, higher accretion rate on the surface of the glomerular epithelial cell. The differential handling of the antibodies by the glomerular epithelial cell offers an explanation for the in vivo differences in the nephritogenicity of these antibodies observed earlier.

Indexed as

Antigen-Antibody ComplexAnimalsAntibodies, MonoclonalAutoantibodiesAutoantigensBasement MembraneCells, CulturedElectrophoresis, Polyacrylamide GelEndocytosisEpitheliumFluorescent Antibody TechniqueGlomerulonephritisImmunohistochemistryKidney GlomerulusMembrane ProteinsMicroscopy, ImmunoelectronAntibodies, MonoclonalAntigen-Antibody ComplexAutoantibodiesAutoantigensMembrane Proteins

Identifiers

PMID8252800
PMCPMC1534444
OpenAlexW2069949675

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.