Evidence map›Paper›PMID 40295683›Full record

ArticleScientific reports2025

Elevated Fab glycosylation of autoantibodies maintained during B cell depletion therapy.

Anika M Valk, Jana Koers, Ninotska I L Derksen, Laura Hogenboom, Zoé van Kempen, Joep Killestein, Abraham Rutgers, Peter Heeringa, Barbara Horváth, Taco W Kuijpers and 7 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Antibody glycosylation in neuroimmune diseases.Journal of translational medicine · 2025
    Review
  3. 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

17 authors.

Anika M ValkDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, Plesmanlaan 125, 1066 CX, Amsterdam, The Netherlands.
Jana KoersDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, Plesmanlaan 125, 1066 CX, Amsterdam, The Netherlands.
Ninotska I L DerksenDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, Plesmanlaan 125, 1066 CX, Amsterdam, The Netherlands.
Laura HogenboomMS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands.
Zoé van KempenMS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands.
Joep KillesteinMS Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam Neuroscience, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands.
Abraham RutgersDepartment of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, The Netherlands.
Peter HeeringaThe Department of Pathology and Medical Biology, University Medical Center Groningen and University of Groningen, Groningen, The Netherlands.
Barbara HorváthDepartment of Dermatology, Groningen Expertise Center for Blistering Diseases, University Medical Center, University Medical Center Groningen, Groningen, The Netherlands.
Taco W KuijpersAmsterdam Institute for Infection and Immunity, Amsterdam, The Netherlands.
S Marieke van HamDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, Plesmanlaan 125, 1066 CX, Amsterdam, The Netherlands.
Anja Ten BrinkeDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, Plesmanlaan 125, 1066 CX, Amsterdam, The Netherlands.
Diane van der WoudeDepartment of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands.
René E M ToesDepartment of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands.
Nicolaas A BosDepartment of Rheumatology and Clinical Immunology, University Medical Center Groningen, Groningen, The Netherlands.
Theo RispensDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam University Medical Center, Plesmanlaan 125, 1066 CX, Amsterdam, The Netherlands. t.rispens@sanquin.nl.
T2B consortium

Funding

Landsteiner Foundation for Blood Transfusion Research Grant1626Samenwerkende Gezondheidsfondsen (SGF) LSHM18055-SGF
6 · The paper itself

Abstract

Several chronic autoimmune diseases are characterized by elevated autoantibody Fab glycosylation. Whether Fab glycans link to disease state or development remains unclear, yet may serve as a marker thereof. Many autoimmune diseases are treated with B cell depletion therapies that particularly result in a decline of autoantibodies. The question arises whether B cell depletion therapy may have an impact on Fab glycosylation. Here, we investigated the longitudinal effects of B cell depletion therapy on Fab glycosylation of total IgG and IgG autoantibodies in rheumatoid arthritis (RA), pemphigus vulgaris (PV), ANCA-associated vasculitis (AAV), and multiple sclerosis (MS). Baseline Fab glycosylation was compared to 6-12 months into therapy by lectin affinity chromatography, determining Fab sialylation as an estimate of Fab glycosylation. We observed a modest decrease in Fab glycosylation of total IgG for RA (median 13.8%[IQR 11.7-16.3] - 9.1%[IQR8-11]) and PV (16.4%[IQR14.9-17.5] - 13.01%[IQR10.8-15.5]) after 6 months, whereas for AAV Fab glycosylation slightly increased (11.6%[IQR7.4-15] - 14.9%[IQR11.4-19.3]), and no changes were found for MS. Autoantibody titers (anti-CCP, anti-PR3, anti-Dsg3) had declined following B cell depletion therapy, yet their elevated Fab glycosylation levels were maintained. Taken together, Fab glycosylation levels of autoantibodies do not decrease upon B cell depletion therapy, thereby retaining their predictive potential as biomarker.

Indexed as

AutoantibodiesAutoimmune DiseasesB-LymphocytesImmunoglobulin Fab FragmentsLymphocyte DepletionAdultAgedArthritis, RheumatoidFemaleGlycosylationHumansImmunoglobulin GMaleMiddle AgedAutoantibodiesImmunoglobulin Fab FragmentsImmunoglobulin GB cell depletion therapyChanges in Fab glycosylation of total IgG compartment upon B cell depletion therapy in autoantibody-mediated chronic autoimmune diseasesChronic autoimmunityFab glycosylation autoantibodiesHigh Fab glycosylation of autoantibodies maintained during B cell depletion therapy

Identifiers

PMID40295683
PMCPMC12037893

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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.