Evidence map›Paper›PMID 20631181›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Passive transfer of IgG anti-GM1 antibodies impairs peripheral nerve repair.

Pablo H Lopez, Gang Zhang, Jiangyang Zhang, Helmar C Lehmann, John W Griffin, Ronald L Schnaar, Kazim A Sheikh

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Observational
  3. Article
  4. Article
  5. Immune-Mediated Neuropathies: Pathophysiology and Management.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Review
  8. Review
  9. Role of Fcγ Receptor Mediated Inflammation in Immune Neuropathies.Journal of clinical & cellular immunology · 2017
    Article
  10. Review
  11. Anti-Ganglioside Antibodies Induce Nodal and Axonal Injury via Fcγ Receptor-Mediated Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  12. Neu3 sialidase-mediated ganglioside conversion is necessary for axon regeneration and is blocked in CNS axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Anti-ganglioside antibody-mediated activation of RhoA induces inhibition of neurite outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  18. 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 2 institutions in 1 country.

Pablo H LopezDepartment of Neurology, The Johns Hopkins University, Baltimore, Maryland 21287, USA.
Gang Zhang
Jiangyang Zhang
Helmar C Lehmann
John W Griffin
Ronald L Schnaar
Kazim A Sheikh
Johns Hopkins University · USThe University of Texas Health Science Center at Houston · US

Funding

Pathogenesis of Anti-ganglioside Antibody-Mediated NeuropathiesR01NS042888 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SHEIKH, KAZIM A · 2002 to 2016
$4.1M
Biologic effects of anti-ganglisiode antibodiesR01NS054962 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SHEIKH, KAZIM A · 2007 to 2018
$3.3M
Complex Carbohydrates in Neuronal Cell FunctionR37NS037096 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCHNAAR, RONALD L · 2005 to 2011
$2.8M
NINDS NIH HHS NS42888NINDS NIH HHS NS54962NINDS NIH HHS R01 NS042888NINDS NIH HHS R01 NS054962NINDS NIH HHS R37 NS037096
6 · The paper itself

Abstract

Anti-GM1 antibodies are present in some patients with autoimmune neurological disorders. These antibodies are most frequently associated with acute immune neuropathy called Guillain-Barré syndrome (GBS). Some clinical studies associate the presence of these antibodies with poor recovery in GBS. The patients with incomplete recovery have failure of nerve repair, particularly axon regeneration. Our previous work indicates that monoclonal antibodies can inhibit axon regeneration by engaging cell surface gangliosides (Lehmann et al., 2007). We asked whether passive transfer of human anti-GM1 antibodies from patients with GBS modulate axon regeneration in an animal model. Human anti-GM1 antibodies were compared with other GM1 ligands, cholera toxin B subunit and a monoclonal anti-GM1 antibody. Our results show that patient derived anti-GM1 antibodies and cholera toxin beta subunit impair axon regeneration/repair after PNS injury in mice. Comparative studies indicated that the antibody/ligand-mediated inhibition of axon regeneration is dependent on antibody/ligand characteristics such as affinity-avidity and fine specificity. These data indicate that circulating immune effectors such as human autoantibodies, which are exogenous to the nervous system, can modulate axon regeneration/nerve repair in autoimmune neurological disorders such as GBS.

Indexed as

Peripheral Nerve InjuriesAnalysis of VarianceAnimalsAntibodies, Anti-IdiotypicAutoantibodiesElectrophysiologyGangliosidesHumansImmunohistochemistryMagnetic Resonance ImagingMiceNerve RegenerationPeripheral NervesAntibodies, Anti-Idiotypicanti-IgGAutoantibodiesGangliosides

Identifiers

PMID20631181
PMCPMC3038609
OpenAlexW2013702603

What OpenQuestion holds

Textmetadata
LicenceTDM
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.