Evidence map›Paper›PMID 10393701›Full record

ArticleThe Journal of clinical investigation1999

Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies.

M Tomana, J Novak, B A Julian, K Matousovic, K Konecny, J Mestecky

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 251 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
251citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

251 citing papers in PubMed, 1 synthesis or guideline pooled it, 476 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. A Rare Genetic Defect ofFrontiers in immunology · 2019
    Trial
  4. Trial
  5. Trial
  6. Review
  7. Review
  8. Review
  9. Nephrin autoimmunity: signal, noise, and a path to clarity.The Journal of clinical investigation · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026
    Review
  17. Review
  18. Review
  19. Review
  20. Review

191 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

M TomanaDepartment of Medicine, Division of Clinical Immunology and Rheumatology, The University of Alabama-Birmingham, Birmingham, Alabama 35294-2041, USA. mtomana@uab.campuscwix.net
J Novak
B A Julian
K Matousovic
K Konecny
J Mestecky
University of Alabama at Birmingham · USCenter for Rheumatology · USCharles University · CZPalacký University Olomouc · CZ

Funding

MOLECULAR ABERRANCIES OF IGA IN IGA NEPHROPATHYR01DK049358 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TOMANA, MILAN · 1994 to 2001
$72k
NIDDK NIH HHS DK-49358
6 · The paper itself

Abstract

Circulating immune complexes (CICs) isolated from sera of patients with IgA nephropathy (IgAN) consist of undergalactosylated, mostly polymeric, and J chain-containing IgA1 and IgG antibodies specific for N-acetylgalactosamine (GalNAc) residues in O-linked glycans of the hinge region of IgA1 heavy chains. Antibodies with such specificity occur in sera of IgAN patients, and in smaller quantities in patients with non-IgA proliferative glomerulonephritis and in healthy controls; they are present mainly in the IgG (predominantly IgG2 subclass), and less frequently in the IgA1 isotype. Their specificity for GalNAc was determined by reactivity with IgA1 myeloma proteins with enzymatically removed N-acetylneuraminic acid (NeuNAc) and galactose (Gal); removal of the O-linked glycans of IgA1 resulted in significantly decreased reactivity. Furthermore, IgA2 proteins that lack the hinge region with O-linked glycans but are otherwise structurally similar to IgA1 did not react with IgG or IgA1 antibodies. The re-formation of isolated and acid-dissociated CICs was inhibited more effectively by IgA1 lacking NeuNAc and Gal than by intact IgA1. Immobilized GalNAc and asialo-ovine submaxillary mucin (rich in O-linked glycans) were also effective inhibitors. Our results suggest that the deficiency of Gal in the hinge region of IgA1 molecules results in the generation of antigenic determinants containing GalNAc residues that are recognized by naturally occurring IgG and IgA1 antibodies.

Indexed as

AcetylgalactosamineAdultAntibody SpecificityAntigen-Antibody ComplexAutoantibodiesAutoantigensCarbohydrate ConformationCarbohydrate SequenceEpitopesFemaleGalactoseGlomerular MesangiumGlomerulonephritis, IGAGlycosylationHumansImmunoglobulin AAcetylgalactosamineAntigen-Antibody ComplexAutoantibodiesAutoantigensEpitopesGalactoseImmunoglobulin AImmunoglobulin GMyeloma ProteinsNeuraminidasePolysaccharides

Identifiers

PMID10393701
PMCPMC408399
OpenAlexW2026103095

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.