Evidence map›Paper›PMID 10749576›Full record

Trial reportThe Journal of clinical investigation2000

Glatiramer acetate (Copaxone) induces degenerate, Th2-polarized immune responses in patients with multiple sclerosis.

P W Duda, M C Schmied, S L Cook, J I Krieger, D A Hafler

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 2 pooled it
22.7field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 418 citations in OpenAlex.

  1. Analysis of multi-drug cancer nanomedicine.Nature nanotechnology · 2025
    Pooled it
  2. Glatiramer acetate for multiple sclerosis.The Cochrane database of systematic reviews · 2010
    Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Therapeutic Advances in Multiple Sclerosis.Frontiers in neurology · 2022
    Review
  18. A Treatment to Cure Diabetes Using Plant-Based Drug Discovery.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  19. Influence of immunomodulatory drugs on the gut microbiota.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  20. Article

67 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

5 authors at 1 institution in 1 country.

P W DudaLaboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
M C Schmied
S L Cook
J I Krieger
D A Hafler
Brigham and Women's Hospital · US

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI David A. Hafler · 1996 to 2026
$51.7M
The function of T Bet in EAEP01NS038037 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2000 to 2010
$12.8M
T CELLS IN THE CSF OF MULTIPLE SCLEROSIS PATIENTSR01NS024247 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI HAFLER, DAVID A. · 1987 to 2003
$1.2M
NIAID NIH HHS P01 AI039671NIAID NIH HHS P01AI39671NINDS NIH HHS P01 NS038037NINDS NIH HHS P01NS38037NINDS NIH HHS R01NS2424710
6 · The paper itself

Abstract

We examined the effect of glatiramer acetate, a random copolymer of alanine, lysine, glutamic acid, and tyrosine, on antigen-specific T-cell responses in patients with multiple sclerosis (MS). Glatiramer acetate (Copaxone) functioned as a universal antigen, inducing proliferation, independent of any prior exposure to the polymer, in T-cell lines prepared from MS or healthy subjects. However, for most patients, daily injections of glatiramer acetate abolished this T-cell response and promoted the secretion of IL-5 and IL-13, which are characteristic of Th2 cells. The surviving glatiramer acetate-reactive T cells exhibited a greater degree of degeneracy as measured by cross-reactive responses to combinatorial peptide libraries. Thus, it appears that, in some individuals, in vivo administration of glatiramer acetate induces highly cross-reactive T cells that secrete Th2 cytokines. To our knowledge, glatiramer acetate is the first agent that suppresses human autoimmune disease and alters immune function by engaging the T-cell receptor. This compound may be useful in a variety of autoimmune disorders in which immune deviation to a Th2 type of response is desirable.

Indexed as

AdultAmino Acid SequenceCell DivisionCells, CulturedCross ReactionsEpitopes, T-LymphocyteFemaleGlatiramer AcetateHumansImmunodominant EpitopesImmunosuppressive AgentsInterferon-gammaInterleukin-5Leukocytes, MononuclearLigandsMaleEpitopes, T-LymphocyteGlatiramer AcetateImmunodominant EpitopesImmunosuppressive AgentsInterferon-gammaInterleukin-5LigandsMyelin Basic Proteinmyelin basic protein 84-102Peptide FragmentsPeptidesTetanus Toxoid

Identifiers

PMID10749576
PMCPMC377485
OpenAlexW2171907184

What OpenQuestion holds

Textmetadata
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.