Evidence map›Paper›PMID 27208700›Full record

ArticleExperimental neurology2016

Sialylated intravenous immunoglobulin suppress anti-ganglioside antibody mediated nerve injury.

Gang Zhang, Cynthia A Massaad, Tong Gao, Laila Pillai, Natalia Bogdanova, Sameera Ghauri, Kazim A Sheikh

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Molecular determinants of sialylated IgG anti-inflammatory activity.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  7. Observational
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  13. Article
  14. IgG Charge: Practical and Biological Implications.Antibodies (Basel, Switzerland) · 2019
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  16. Article
  17. Review
  18. Article
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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 1 institution in 1 country.

Gang Zhang *Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
Cynthia A Massaad *Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
Tong GaoDepartment of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
Laila PillaiDepartment of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
Natalia BogdanovaDepartment of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
Sameera GhauriDepartment of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
Kazim A SheikhDepartment of Neurology, University of Texas Medical School at Houston, 6431 Fannin street, Houston, Texas 77030.
The 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
Modulation of FcRn: A strategy to prevent autoantibody-mediated nerve injuryR21NS087467 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SHEIKH, KAZIM A · 2014 to 2015
$380k
NINDS NIH HHS R01 NS042888NINDS NIH HHS R01 NS054962NINDS NIH HHS R21 NS087467
6 · The paper itself

Abstract

The precise mechanisms underlying the efficacy of intravenous immunoglobulin (IVIg) in autoimmune neurological disorders including Guillain-Barré syndrome (GBS) are not known. Anti-ganglioside antibodies have been reported to be pathogenic in some variants of GBS, and we have developed passive transfer animal models to study anti-ganglioside antibody mediated-endoneurial inflammation and associated neuropathological effects and to evaluate the efficacy of new therapeutic approaches. Some studies indicate that IVIg's anti-inflammatory activity resides in a minor sialylated IVIg (sIVIg) fractions and is dependent on an innate Th2 response via binding to a specific ICAM3-grabbing nonintegrin related 1 receptor (SIGN-R1). Therefore the efficacy of IVIg, IVIg fractions with various IgG Fc sialylation status, and the involvement of Th2 pathway were examined in one of our animal model of antibody-mediated inhibition of axonal regeneration. We demonstrate that both IVIg and sIVIg ameliorated anti-glycan antibody mediated-pathological effect, whereas, the unsialylated fractions of IVIg were not beneficial in our model. Tenfold lower doses of sIVIg compared to whole IVIg provided equivalent efficacy in our studies. Moreover, we found that whole IVIg and sIVIg significantly upregulates the gene expression of IL-33, which itself can provide protection from antibody-mediated nerve injury in our model. Our results support that the SIGN-R1-Th2 pathway is involved in the anti-inflammatory effects of IVIg on endoneurium in our model and elements of this pathway including IL-33 can provide novel therapeutics in inflammatory neuropathies.

Indexed as

AnimalsAntibodiesDisease Models, AnimalDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayGangliosidesGene Expression RegulationGuillain-Barre SyndromeImmunoglobulins, IntravenousImmunologic FactorsInterleukin-33MiceMice, Inbred C57BLNerve RegenerationRecovery of FunctionRNA, MessengerAntibodiesGangliosidesImmunoglobulins, IntravenousImmunologic FactorsInterleukin-33RNA, MessengerGuillain-Barré syndromeIL-33IL-4IVIgSIGN-R1sIVIgTh2 pathway

Identifiers

PMID27208700
PMCPMC5351292
OpenAlexW2396047646

What OpenQuestion holds

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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.