Evidence map›Paper›PMID 20448018›Full record

ArticleJournal of the American Society of Nephrology : JASN2010

IgG glycan hydrolysis attenuates ANCA-mediated glomerulonephritis.

Mirjan M van Timmeren, Betty S van der Veen, Coen A Stegeman, Arjen H Petersen, Thomas Hellmark, Mattias Collin, Peter Heeringa

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Glycosylation Profile of IgG in Moderate Kidney Dysfunction.Journal of the American Society of Nephrology : JASN · 2016
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Immunomodulating Enzymes fromMicroorganisms · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Association of the IgGBMJ open diabetes research & care · 2020
    Article
  13. Review
  14. Review
  15. Animal Models of ANCA Associated Vasculitis.Frontiers in immunology · 2020
    Review
  16. Article
  17. Article
  18. Emerging immunotherapies for autoimmune kidney disease.Human vaccines & immunotherapeutics · 2019
    Review
  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

7 authors at 4 institutions in 3 countries.

Mirjan M van TimmerenDepartments of Pathology and Medical Biology, University Medical Center Groningen and University of Groningen, Groningen, Netherlands.
Betty S van der Veen
Coen A Stegeman
Arjen H Petersen
Thomas Hellmark
Mattias Collin
Peter Heeringa
Hanze University of Applied Sciences · NLLund University · SEPediatric Nephrology of Alabama · USUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-neutrophil cytoplasmic autoantibodies (ANCA) directed against myeloperoxidase (MPO) and proteinase 3 (Pr3) are considered pathogenic in ANCA-associated necrotizing and crescentic glomerulonephritis (NCGN) and vasculitis. Modulation of ANCA IgG glycosylation may potentially reduce its pathogenicity by abolishing Fc receptor-mediated activation of leukocytes and complement. Here, we investigated whether IgG hydrolysis by the bacterial enzyme endoglycosidase S (EndoS) attenuates ANCA-mediated NCGN. In vitro, treatment of ANCA IgG with EndoS significantly attenuated ANCA-mediated neutrophil activation without affecting antigen-binding capacity. In a mouse model of anti-MPO IgG/LPS-induced NCGN, we induced disease with either unmodified or EndoS-treated (deglycosylated) anti-MPO IgG. In separate experiments, we administered EndoS systemically after disease induction with unmodified anti-MPO IgG. Pretreatment of anti-MPO IgG with EndoS reduced hematuria, leukocyturia, and albuminuria and attenuated both neutrophil influx and formation of glomerular crescents. After inducing disease with unmodified anti-MPO IgG, systemic treatment with EndoS reduced albuminuria and glomerular crescent formation when initiated after 3 but not 24 hours. In conclusion, IgG glycan hydrolysis by EndoS attenuates ANCA-induced neutrophil activation in vitro and prevents induction of anti-MPO IgG/LPS-mediated NCGN in vivo. Systemic treatment with EndoS early after disease induction attenuates the development of disease. Thus, modulation of IgG glycosylation is a promising strategy to interfere with ANCA-mediated inflammatory processes.

Indexed as

AdultAgedAnimalsAntibodies, Antineutrophil CytoplasmicBacterial ProteinsCase-Control StudiesDisease Models, AnimalFemaleGlomerulonephritisGlycoside HydrolasesHumansHydrolysisImmunoglobulin GLipopolysaccharidesMaleMiceAntibodies, Antineutrophil CytoplasmicBacterial ProteinsGlycoside HydrolasesImmunoglobulin GLipopolysaccharidesNDOS protein, Streptococcus pyogenesPeroxidasePolysaccharides

Identifiers

PMID20448018
PMCPMC3152232
OpenAlexW2166599546

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.