Evidence map›Paper›PMID 15308777›Full record

ReviewProceedings of the National Academy of Sciences of the United States of America2004

Therapeutic vaccines in autoimmunity.

Michael Sela, Edna Mozes

Open access · greenAbstract readReview
In one paragraph

Review in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 47 citations in OpenAlex.

  1. Vaccines in Breast Cancer: Challenges and Breakthroughs.Diagnostics (Basel, Switzerland) · 2023
    Review
  2. Article
  3. Review
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  5. Article
  6. Review
  7. Review
  8. Article
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  10. Review
  11. Multimerized T cell epitopes protect from experimental autoimmune diabetes by inducing dominant tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  12. Article
  13. Does inflammation in an autoimmune disease differ from inflammation in neurodegenerative diseases? Possible implications for therapy.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2006
    Review
  14. Vaccines against myasthenia gravis.Expert opinion on biological therapy · 2005
    Review
  15. Article
  16. 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

2 authors at 1 institution in 1 country.

Michael SelaDepartment of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. michael.sela@weizmann.ac.il
Edna Mozes
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Similarly to prophylactic vaccines whose purpose is to prevent infectious diseases, therapeutic vaccines against autoimmune diseases are based on their similarity to the putative causes of the disease. We shall describe here two such examples: a copolymer of amino acids related to myelin basic protein, in the case of multiple sclerosis, and a peptide derived from the nicotinic acetylcholine receptor (AChR), in the case of myasthenia gravis (MG). Copolymer 1 (Cop 1, glatiramer acetate, Copaxone) is a synthetic amino acid random copolymer, immunologically cross-reactive with myelin basic protein and suppresses experimental allergic encephalomyelitis in several animal species. Cop 1 slows the progression of disability and reduces relapse rate in exacerbating-remitting multiple sclerosis patients. It was approved by the Food and Drug Administration in 1996, and today is used by tens of thousands of patients. Cop 1 is a potent inducer of T helper 2 (Th2) regulatory cells in mice and humans, and Th2 cells are found both in the brains and spinal cords of Cop 1-treated mice. MG and experimental autoimmune MG are T cell-regulated, antibody-mediated autoimmune diseases. Two peptides, representing sequences of the human AChR alpha-subunit, p195-212 and p259-271, are immunodominant T cell epitopes in MG patients and in two strains of mice. Altered peptide ligand, composed of the tandemly arranged two single amino acid analogs, inhibits in vitro and in vivo MG-associated autoimmune responses. The active suppression is mediated by the CD4(+)CD25(+) immunoregulatory cells and is associated with the down-regulation of Th1-type cytokines and the up-regulation of the secretion of IL-10 and the immunosuppressive cytokine, transforming growth factor beta.

Indexed as

AnimalsAutoimmune DiseasesClonal AnergyCytokinesEncephalomyelitis, Autoimmune, ExperimentalGlatiramer AcetateHumansMatrix Metalloproteinase 9MiceMultiple SclerosisMyasthenia GravisPeptidesReceptors, NicotinicT-LymphocytesType C PhospholipasesVaccinesCytokinesGlatiramer AcetateMatrix Metalloproteinase 9PeptidesReceptors, NicotinicType C PhospholipasesVaccines

Identifiers

PMID15308777
PMCPMC521984
OpenAlexW1997105425

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.