Evidence map›Paper›PMID 25152896›Full record

ReviewJournal of immunology research2014

Cellular signaling and production of galactose-deficient IgA1 in IgA nephropathy, an autoimmune disease.

Colin Reily, Hiroyuki Ueda, Zhi-Qiang Huang, Jiri Mestecky, Bruce A Julian, Christopher D Willey, Jan Novak

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Cytokines and Production of AberrantlyJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. The Emerging Role of Pathogenesis of IgA Nephropathy.Journal of clinical medicine · 2018
    Review
  11. Article
  12. Article
  13. Review
  14. 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

7 authors at 1 institution in 1 country.

Colin ReilyDepartment of Microbiology, University of Alabama at Birmingham, 845 19th Street South, BBRB 762, Birmingham, AL 35294, USA.ORCID 0000-0002-4033-1360
Hiroyuki UedaDepartment of Microbiology, University of Alabama at Birmingham, 845 19th Street South, BBRB 762, Birmingham, AL 35294, USA.ORCID 0000-0002-8282-7313
Zhi-Qiang HuangDepartment of Microbiology, University of Alabama at Birmingham, 845 19th Street South, BBRB 762, Birmingham, AL 35294, USA.
Jiri MesteckyDepartment of Microbiology, University of Alabama at Birmingham, 845 19th Street South, BBRB 762, Birmingham, AL 35294, USA ; Department of Medicine, University of Alabama at Birmingham, 845 19th Street South, Birmingham, AL 35294, USA.
Bruce A JulianDepartment of Microbiology, University of Alabama at Birmingham, 845 19th Street South, BBRB 762, Birmingham, AL 35294, USA ; Department of Medicine, University of Alabama at Birmingham, 845 19th Street South, Birmingham, AL 35294, USA.
Christopher D WilleyDepartment of Radiation Oncology, University of Alabama at Birmingham, 845 19th Street South, Birmingham, AL 35294, USA.ORCID 0000-0001-9953-0279
Jan NovakDepartment of Microbiology, University of Alabama at Birmingham, 845 19th Street South, BBRB 762, Birmingham, AL 35294, USA.ORCID 0000-0002-9211-6670
University of Alabama at Birmingham · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
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
TRAINING IN CELLULAR PHYSIOLOGY MEMBRANE TRANSPORTT32DK007545 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GUTIERREZ, ORLANDO M · 1987 to 2023
$4.5M
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
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 DK078244NIDDK NIH HHS DK082753NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK078244NIDDK NIH HHS R01 DK082753NIDDK NIH HHS R56 DK078244NIDDK NIH HHS T32 DK007545NIDDK NIH HHS T32DK079337NIGMS NIH HHS GM098539NIGMS NIH HHS R01 GM098539
6 · The paper itself

Abstract

Immunoglobulin A (IgA) nephropathy (IgAN), the leading cause of primary glomerulonephritis, is characterized by IgA1-containing immunodeposits in the glomeruli. IgAN is a chronic disease, with up to 40% of patients progressing to end-stage renal disease, with no disease-specific treatment. Multiple studies of the origin of the glomerular immunodeposits have linked elevated circulating levels of aberrantly glycosylated IgA1 (galactose-deficient in some O-glycans; Gd-IgA1) with formation of nephritogenic Gd-IgA1-containing immune complexes. Gd-IgA1 is recognized as an autoantigen in susceptible individuals by anti-glycan autoantibodies, resulting in immune complexes that may ultimately deposit in the kidney and induce glomerular injury. Genetic studies have revealed that an elevated level of Gd-IgA1 in the circulation of IgAN patients is a hereditable trait. Moreover, recent genome-wide association studies have identified several immunity-related loci that associated with IgAN. Production of Gd-IgA1 by IgA1-secreting cells of IgAN patients has been attributed to abnormal expression and activity of several key glycosyltransferases. Substantial evidence is emerging that abnormal signaling in IgA1-producing cells is related to the production of Gd-IgA1. As Gd-IgA1 is the key autoantigen in IgAN, understanding the genetic, biochemical, and environmental aspects of the abnormal signaling in IgA1-producing cells will provide insight into possible targets for future disease-specific therapy.

Indexed as

Signal TransductionAnimalsAutoimmune DiseasesGalactoseGenetic LociGenetic Predisposition to DiseaseGenome-Wide Association StudyGlomerulonephritis, IGAGlycosylationGlycosyltransferasesHumansImmunoglobulin AGalactoseGlycosyltransferasesImmunoglobulin A

Identifiers

PMID25152896
PMCPMC4134797
OpenAlexW2044833572

What OpenQuestion holds

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Registered trials

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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.