Evidence map›Paper›PMID 21476611›Full record

ReviewCNS drugs2011

Glatiramer acetate in the treatment of multiple sclerosis: emerging concepts regarding its mechanism of action.

Patrice H Lalive, Oliver Neuhaus, Mahdia Benkhoucha, Danielle Burger, Reinhard Hohlfeld, Scott S Zamvil, Martin S Weber

Abstract readReview
In one paragraph

Review in CNS drugs, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
9.8field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 171 citations in OpenAlex.

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  17. Drug-induced liver injury by glatiramer acetate leading to liver transplant: A case report.JGH open : an open access journal of gastroenterology and hepatology · 2023
    Article
  18. Review
  19. Review
  20. Article

29 more citing papers are in PubMed but not listed here.

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 5 institutions in 3 countries.

Patrice H LaliveDepartment of Neurosciences, Geneva University Hospital and University of Geneva, Geneva, Switzerland.
Oliver Neuhaus
Mahdia Benkhoucha
Danielle Burger
Reinhard Hohlfeld
Scott S Zamvil
Martin S Weber
University Hospital of Geneva · CHLudwig-Maximilians-Universität München · DETechnical University of Munich · DEUniversity of California, San Francisco · USUniversity of Geneva · CH

Funding

Immunomodulation of inflammatory disease by atorvastatinR01AI059709 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAMVIL, SCOTT S · 2005 to 2009
$2.1M
B cells in CNS autoimmunityR01AI073737 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAMVIL, SCOTT S · 2009 to 2013
$1.9M
Regulatory monocytes in CNS autoimmune diseaseR01NS063008 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ZAMVIL, SCOTT S · 2009 to 2013
$1.3M
NIAID NIH HHS R01 AI059709NIAID NIH HHS R01 AI073737NINDS NIH HHS R01 NS063008
6 · The paper itself

Abstract

Glatiramer acetate is a synthetic, random copolymer widely used as a first-line agent for the treatment of relapsing-remitting multiple sclerosis (MS). While earlier studies primarily attributed its clinical effect to a shift in the cytokine secretion of CD4+ T helper (T(h)) cells, growing evidence in MS and its animal model, experimental autoimmune encephalomyelitis (EAE), suggests that glatiramer acetate treatment is associated with a broader immunomodulatory effect on cells of both the innate and adaptive immune system. To date, glatiramer acetate-mediated modulation of antigen-presenting cells (APC) such as monocytes and dendritic cells, CD4+ T(h) cells, CD8+ T cells, Foxp3+ regulatory T cells and antibody production by plasma cells have been reported; in addition, most recent investigations indicate that glatiramer acetate treatment may also promote regulatory B-cell properties. Experimental evidence suggests that, among these diverse effects, a fostering interplay between anti-inflammatory T-cell populations and regulatory type II APC may be the central axis in glatiramer acetate-mediated immune modulation of CNS autoimmune disease. Besides altering inflammatory processes, glatiramer acetate could exert direct neuroprotective and/or neuroregenerative properties, which could be of relevance for the treatment of MS, but even more so for primarily neurodegenerative disorders, such as Alzheimer's or Parkinson's disease. In this review, we provide a comprehensive and critical overview of established and recent findings aiming to elucidate the complex mechanism of action of glatiramer acetate.

Indexed as

AnimalsDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGlatiramer AcetateHumansImmunosuppressive AgentsMaleMiceMultiple SclerosisMultiple Sclerosis, Relapsing-RemittingNeuroprotective AgentsPeptidesGlatiramer AcetateImmunosuppressive AgentsNeuroprotective AgentsPeptides

Identifiers

PMID21476611
PMCPMC3963480
OpenAlexW1990785469

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.