Evidence map›Paper›PMID 36999029›Full record

ArticleFrontiers in immunology2023

Effect of monovalency on anti-contactin-1 IgG4.

Guillaume Taieb, Alexandre Jentzer, Elisa Vegezzi, Cinta Lleixà, Isabel Illa, Luis Querol, Jérôme J Devaux

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Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Antibody-Mediated Nodo- and Paranodopathies.Journal of clinical medicine · 2024
    Review
  6. Review
  7. 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.

Guillaume TaiebInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Alexandre JentzerInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Elisa VegezziDepartment of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy.
Cinta LleixàNeuromuscular Diseases Unit, Hospital de la Santa Creu i Sant Pau, Universitat Autónoma de Barcelona, Barcelona, Spain.
Isabel IllaNeuromuscular Diseases Unit, Hospital de la Santa Creu i Sant Pau, Universitat Autónoma de Barcelona, Barcelona, Spain.
Luis QuerolNeuromuscular Diseases Unit, Hospital de la Santa Creu i Sant Pau, Universitat Autónoma de Barcelona, Barcelona, Spain.
Jérôme J DevauxInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Autoimmune nodopathies (AN) have been diagnosed in a subset of patients fulfilling criteria for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) who display no or poor response to intravenous immunoglobulins. Biomarkers of AN are autoantibodies, mainly IgG4, directed against the ternary paranodal complex composed by neurofascin-155, contactin-1 (CNTN1), and Contactin-associated-protein-1 (CASPR1) or against the nodal isoforms of neurofascin. IgG4 can undergo a Fab-arm exchange (FAE) which results in functionally monovalent antibody. This phenomenon differentially affects the pathogenicity of IgG4 depending on the target of autoantibodies. Here, we have evaluated this issue by examining the impact of valency on anti-CNTN1 IgG4 which induces paranodal destruction through a function blocking activity. Methods: Sera were obtained from 20 patients with AN associated with anti-CNTN1 antibodies. The proportion of monospecific/bispecific anti-CNTN1 antibodies was estimated in each patient by ELISA by examining the ability of serum antibodies to cross-link untagged CNTN1 with biotinylated CNTN1. To determine the impact of monovalency, anti-CNTN1 IgG4 were enzymatically digested into monovalent Fab and tested Results and discussion: We found that the percentage of monospecific antibodies were lower than 5% in 14 out of 20 patients (70%), suggesting that IgG4 have undergone extensive FAE

Indexed as

Antibodies, BispecificImmunoglobulin GAutoantibodiesCell Adhesion MoleculesContactin 1Nerve Growth FactorsAntibodies, BispecificAutoantibodiesCell Adhesion MoleculesContactin 1Immunoglobulin GNerve Growth Factorsauto-immuneaxondemyelinationGBSimmunoglobulinmyelinSchwann

Identifiers

PMID36999029
PMCPMC10045471

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