Evidence map›Paper›PMID 25288571›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Antigen-specific immunotherapeutic vaccine for experimental autoimmune myasthenia gravis.

Jie Luo, Jon Lindstrom

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Advances in autoimmune myasthenia gravis management.Expert review of neurotherapeutics · 2018
    Review
  6. Article
  7. Co-delivery of autoantigen and dexamethasone in incomplete Freund's adjuvant ameliorates experimental autoimmune encephalomyelitis.Journal of controlled release : official journal of the Controlled Release Society · 2017
    Article
  8. Article
  9. Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017
    Review
  10. Review
  11. Current Treatment, Emerging Translational Therapies, and New Therapeutic Targets for Autoimmune Myasthenia Gravis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  12. Article
  13. Caspr2 autoantibodies target multiple epitopes.Neurology(R) neuroimmunology & neuroinflammation · 2015
    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.

Jie LuoDepartment of Neuroscience, University of Pennsylvania Medical School, Philadelphia, PA 19104.
Jon LindstromDepartment of Neuroscience, University of Pennsylvania Medical School, Philadelphia, PA 19104 jslkk@mail.med.upenn.edu.
University of Pennsylvania · US

Funding

EAMG: MIR structure and specific immunosuppressive therapyR01NS052463 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI LINDSTROM, JON MARTIN · 2006 to 2009
$1.7M
NINDS NIH HHS R01 NS052463
6 · The paper itself

Abstract

Myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG) are caused by Ab-mediated autoimmune responses to muscle nicotinic acetylcholine receptors (AChRs) that impair neuromuscular transmission, thereby causing muscle weakness. Previously, we discovered that i.p. injection of a therapeutic vaccine consisting of bacterially expressed cytoplasmic domains of human AChR subunits reduced the development of chronic EAMG in rats. In this article, we show that immunization with the therapeutic vaccine in adjuvants does not induce EAMG and, thus, is safe. The potency and efficacy of the therapeutic vaccine were greatly increased by s.c. administration of repeated low doses in IFA. Onset of chronic EAMG could be prevented. Established chronic EAMG could be rapidly reversed, modeling therapy of chronic MG. Therapy reduced pathological Abs assayed by immune precipitation of a main immunogenic region chimera. Successfully treated rats exhibited long-term resistance to reinduction of EAMG, suggesting a lasting cure of MG. A long-term effect of therapy was to change the isotype of the pathogenic Ab response from IgG2b, which fixes complement, to IgG1, which does not. Prevention and reversal of chronic EAMG was not caused by the isotype switch, but the isotype switch may contribute to resistance to reinduction of EAMG. Immunization with AChR cytoplasmic domains in adjuvant is promising as a safe, Ag-specific, potent, effective, rapidly acting, and long-lasting therapeutic approach to MG.

Indexed as

AnimalsAutoantibodiesFemaleHumansImmunoglobulin Class SwitchingImmunoglobulin GInjections, SubcutaneousMusclesMyasthenia Gravis, Autoimmune, ExperimentalProtein SubunitsRatsRats, Inbred LewReceptors, CholinergicRecombinant ProteinsTorpedoVaccinesAutoantibodiesImmunoglobulin GProtein SubunitsReceptors, CholinergicRecombinant ProteinsVaccines

Identifiers

PMID25288571
PMCPMC4273672
OpenAlexW2126519478

What OpenQuestion holds

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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.