Evidence map›Paper›PMID 38961307›Full record

ReviewNature reviews. Nephrology2024

The role of antibody glycosylation in autoimmune and alloimmune kidney diseases.

Anaïs Beyze, Christian Larroque, Moglie Le Quintrec

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Observational
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Therapeutic effect of galactosyltransferase- and sialyltransferase-encoding mRNA in rheumatoid arthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  17. Article
  18. Article
  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

3 authors.

Anaïs BeyzeInstitute of Regenerative Medicine and Biotherapy, IRMB U1183, Montpellier, France. a-beyze@chu-montpellier.fr.ORCID 0009-0009-2637-4020
Christian LarroqueInstitute of Regenerative Medicine and Biotherapy, IRMB U1183, Montpellier, France.
Moglie Le QuintrecInstitute of Regenerative Medicine and Biotherapy, IRMB U1183, Montpellier, France. m-lequintrec-donnette@chu-montpellier.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin glycosylation is a pivotal mechanism that drives the diversification of antibody functions. The composition of the IgG glycome is influenced by environmental factors, genetic traits and inflammatory contexts. Differential IgG glycosylation has been shown to intricately modulate IgG effector functions and has a role in the initiation and progression of various diseases. Analysis of IgG glycosylation is therefore a promising tool for predicting disease severity. Several autoimmune and alloimmune disorders, including critical and potentially life-threatening conditions such as systemic lupus erythematosus, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis and antibody-mediated kidney graft rejection, are driven by immunoglobulin. In certain IgG-driven kidney diseases, including primary membranous nephropathy, IgA nephropathy and lupus nephritis, particular glycome characteristics can enhance in situ complement activation and the recruitment of innate immune cells, resulting in more severe kidney damage. Hypofucosylation, hypogalactosylation and hyposialylation are the most common IgG glycosylation traits identified in these diseases. Modulating IgG glycosylation could therefore be a promising therapeutic strategy for regulating the immune mechanisms that underlie IgG-driven kidney diseases and potentially reduce the burden of immunosuppressive drugs in affected patients.

Indexed as

Immunoglobulin GAutoimmune DiseasesGlycoproteinsGlycosylationGraft RejectionHumansKidney DiseasesGlycoproteinsglycosylated IgGImmunoglobulin G

Identifiers

What OpenQuestion holds

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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.