Evidence map›Paper›PMID 27444044›Full record

ReviewClinical immunology (Orlando, Fla.)2016

IgA nephropathy enigma.

Jiri Mestecky, Jan Novak, Zina Moldoveanu, Milan Raska

Open access · greenAbstract readReview
In one paragraph

Review in Clinical immunology (Orlando, Fla.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  17. Immunoproteasome in IgA Nephropathy: State-of-Art and Future Perspectives.International journal of biological sciences · 2020
    Review
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 2 countries.

Jiri MesteckyUniversity of Alabama at Birmingham, Department of Microbiology, Birmingham, AL, USA; First School of Medicine, Department of Immunology and Microbiology, Charles University, Prague, Czech Republic; Czech Academy of Sciences, Institute of Microbiology, Prague, Czech Republic. Electronic address: mestecky@uab.edu.
Jan NovakUniversity of Alabama at Birmingham, Department of Microbiology, Birmingham, AL, USA.
Zina MoldoveanuUniversity of Alabama at Birmingham, Department of Microbiology, Birmingham, AL, USA.
Milan RaskaUniversity of Alabama at Birmingham, Department of Microbiology, Birmingham, AL, USA; Palacky University, Faculty of Medicine and Dentistry and University Hospital, Department of Immunology, Olomouc, Czech Republic.
University of Alabama at Birmingham · USPalacký University Olomouc · CZ

Funding

Elucidating IgA Nephropathy through Genetic Studies of IgA1 GlycosylationR01DK082753 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GHARAVI, ALI G, NOVAK, JAN · 2009 to 2024
$8.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR01DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAN NOVAK · 2007 to 2026
$6.0M
Genetics of IgA nephropathy by integrative network-based association studiesR01DK105124 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Krzysztof Kiryluk · 2015 to 2026
$4.8M
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
IgA Nephropathy: Interventions with Generation of Nephritogenic Immune ComplexesR01DK099228 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MESTECKY, JIRI F, NOVAK, JAN · 2014 to 2016
$993k
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR56DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NOVAK, JAN · 2012 to 2012
$92k
NIDDK NIH HHS R01 DK078244NIDDK NIH HHS R01 DK082753NIDDK NIH HHS R01 DK099228NIDDK NIH HHS R01 DK105124NIDDK NIH HHS R56 DK078244NIGMS NIH HHS R01 GM098539
6 · The paper itself

Abstract

IgA nephropathy (IgAN) is the leading cause of primary glomerulonephritis in the world. The disease is characterized by the presence of IgA-containing immune complexes in the circulation and in mesangial deposits with ensuing glomerular injury. Although in humans there are two IgA subclasses, only IgA1 molecules are involved. The exclusivity of participation of IgA1 in IgAN prompted extensive structural and immunological studies of the unique hinge region (HR) of IgA1, which is absent in otherwise highly homologous IgA2. HR of IgA1 with altered O-glycans serves as an antigen recognized by autoantibodies specific for aberrant HR glycans leading to the generation of nephritogenic immune complexes. However, there are several unresolved questions concerning the phylogenetic origin of human IgA1 HR, the structural basis of its antigenicity, the origin of antibodies specific for HR with altered glycan moieties, the regulatory defects in IgA1 glycosylation pathways, and the potential approaches applicable to the disease-specific interventions in the formation of nephritogenic immune complexes. This review focuses on the gaps in our knowledge of molecular and cellular events that are involved in the immunopathogenesis of IgAN.

Indexed as

AnimalsDisease Models, AnimalGlomerulonephritis, IGAHumansImmunoglobulin AImmunoglobulin AAnimal models of IgA nephropathyAutoimmunityIgA glycansIgA glycosylationIgA hinge regionIgA nephropathyIgA subclasses

Identifiers

PMID27444044
PMCPMC5159197
OpenAlexW2480204826

What OpenQuestion holds

Textmetadata
LicenceTDM
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.