Evidence map›Paper›PMID 20077429›Full record

ArticleJournal of neuroscience research2010

Novel anti-idiotype antibody therapy for lipooligosaccharide-induced experimental autoimmune neuritis: use relevant to Guillain-Barré syndrome.

S Usuki, K Taguchi, S A Thompson, P B Chapman, R K Yu

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroscience research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Immunoglobulin and Monoclonal Antibody Therapies in Guillain-Barré Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  5. Article
  6. Review
  7. The Promise of Anti-idiotype Revisited.Frontiers in immunology · 2019
    Review
  8. Selective in vivo removal of pathogenic anti-MAG autoantibodies, an antigen-specific treatment option for anti-MAG neuropathy.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Review
  10. New strategies in the management of Guillain-Barré syndrome.Clinical reviews in allergy & immunology · 2014
    Review
  11. Infection and autoimmune disease.Rheumatology international · 2012
    Review
  12. Article
  13. Neuronal dysfunction with aging and its amelioration.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2012
    Review
  14. Article
  15. 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

5 authors at 3 institutions in 2 countries.

S UsukiInstitute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912-2697, USA.
K Taguchi
S A Thompson
P B Chapman
R K Yu
Augusta University · USMemorial Sloan Kettering Cancer Center · USShowa Pharmaceutical University · JP

Funding

ROLE OF GLYCOLIPIDS IN EXPERIMENTAL NEUROPATHYR01NS026994 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI YU, ROBERT K. · 1988 to 2012
$3.3M
NINDS NIH HHS NS26994NINDS NIH HHS R01 NS026994
6 · The paper itself

Abstract

Campylobacteriosis is a frequent antecedent event in Guillain-Barré syndrome (GBS), inducing high-titer serum antibodies for ganglioside antigens in the peripheral nervous system (PNS). Molecular mimicry between the lipooligosaccharide (LOS) component of Campylobacter jejuni and human peripheral nerve gangliosides is believed to play an important role in the pathogenesis of GBS. Conventional treatment strategies for patients with GBS include plasmapheresis, intravenous immunoglobulin (IVIG), and immunosuppression, which are invasive or relatively ineffective. In this study, we used our animal model of GBS, in which Lewis rats were immunized with GD3-like LOS isolated from C.jejuni. The animals developed anti-GD3 ganglioside antibodies and manifested neuromuscular dysfunction. To develop novel therapeutic strategies, we treated the animals by intraperitoneal administration of an anti-GD3 antiidiotype monoclonal antibody (BEC2) that specifically interacts with the pathogenic antibody. The treated animals had a remarkable reduction of anti-GD3 antibody titers and improvement of motor nerve functions. The results suggest that ganglioside mimics, such as antiidiotype antibodies, may be powerful reagents for therapeutic intervention in GBS by neutralizing specific pathogenic antiganglioside antibodies.

Indexed as

Action PotentialsAnimalsAntibodies, Anti-IdiotypicBiotinylationCampylobacter jejuniCoculture TechniquesDisease Models, AnimalDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayEther-A-Go-Go Potassium ChannelsFemaleFreund's AdjuvantGangliosidesLipopolysaccharidesMotor NeuronsMuscle, SkeletalAntibodies, Anti-IdiotypicEther-A-Go-Go Potassium ChannelsFreund's Adjuvantganglioside, GD3GangliosidesKcnh4 protein, ratlipid-linked oligosaccharidesLipopolysaccharidesNerve Tissue Proteins

Identifiers

PMID20077429
PMCPMC3012786
OpenAlexW1973681449

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.