Evidence map›Paper›PMID 18182777›Full record

ReviewKidney & blood pressure research2008

Role of aberrant glycosylation of IgA1 molecules in the pathogenesis of IgA nephropathy.

J Mestecky, M Tomana, Z Moldoveanu, B A Julian, H Suzuki, K Matousovic, M B Renfrow, L Novak, R J Wyatt, J Novak

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney & blood pressure research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
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  14. Representing glycophenotypes: semantic unification of glycobiology resources for disease discovery.Database : the journal of biological databases and curation · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Inflammation in IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2017
    Review
  19. Article
  20. Article
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

10 authors at 4 institutions in 3 countries.

J MesteckyDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294-2170, USA. mestecky@uab.edu
M Tomana
Z Moldoveanu
B A Julian
H Suzuki
K Matousovic
M B Renfrow
L Novak
R J Wyatt
J Novak
Czech Academy of Sciences, Institute of Microbiology · CZUniversity of Alabama at Birmingham · USCharles University · CZUniversity of Tennessee Health Science Center · US

Funding

Zevalin Radioimmunotherapy Using a Modified TreatmentM01RR000032 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RICH, ROBERT R. · 1985 to 2008
$23.6M
Immune Complexes and Mesangial Cells in IGA NephropathyP01DK061525 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MESTECKY, JIRI F · 2002 to 2006
$6.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR01DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAN NOVAK · 2007 to 2026
$6.0M
Analytical tools for the analysis of clustered O-glycans in clinical samplesR01GM098539 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RENFROW, MATTHEW B · 2011 to 2019
$2.7M
IgA1 glycosylation and receptor interactions in IgA nephropathyR01DK071802 · NIDDK · UNIVERSITY OF CINCINNATI · PI HERR, ANDREW B · 2006 to 2010
$1.5M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR56DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NOVAK, JAN · 2012 to 2012
$92k
NCRR NIH HHS M01 RR000032NCRR NIH HHS M01 RR00032NIDDK NIH HHS DK61525NIDDK NIH HHS DK71802NIDDK NIH HHS DK78244NIDDK NIH HHS P01 DK061525NIDDK NIH HHS R01 DK071802NIDDK NIH HHS R01 DK078244NIDDK NIH HHS R56 DK078244NIGMS NIH HHS R01 GM098539
6 · The paper itself

Abstract

Studies of the properties of immune complexes (IC) in the circulation, urine, and mesangium of IgA nephropathy (IgAN) patients have provided data relevant to the pathogenesis of this disease. IC contain predominantly polymeric IgA1 molecules which are deficient in galactose (Gal) residues on O-linked glycan chains in the hinge region (HR) of their heavy (H) chains. As a result of this aberrancy, a novel antigenic determinant(s) involving N-acetylgalactosamine (GalNAc) and perhaps sialic acid (SA) of O-linked glycans is generated and recognized by naturally occurring GalNAc-specific antibodies. Thus, IC in IgAN consist of Gal-deficient IgA1 molecules as an antigen, and GalNAc-specific IgG and/or IgA1 as an antibody. IgG antibodies to Gal-deficient IgA1 are probably induced by cross-reactive microbial antigens; they are present at variable levels not only in humans with or without IgAN but also in many phylogenetically diverse vertebrate species. Incubation of human mesangial cells with IC from sera of IgAN patients indicated that stimulation of cellular proliferative activity was restricted to the large (>800 kDa) complexes. These findings suggest that experimental approaches that prevent the formation of large Gal-deficient IgA1-IgG IC may be applied ultimately in an immunologically mediated therapy.

Indexed as

AnimalsGlomerulonephritis, IGAGlycosylationHumansImmunoglobulin AImmunoglobulin A

Identifiers

PMID18182777
PMCPMC2821435
OpenAlexW2038976546

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.