Evidence map›Paper›PMID 32457737›Full record

ReviewFrontiers in immunology2020

Muscle-Specific Kinase Myasthenia Gravis.

Lucia S Borges, David P Richman

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.8field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Long-term efficacy and safety of tacrolimus in anti-MuSK antibody-positive myasthenia gravis: a retrospective single-center cohort study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Therapeutic advances of targeting receptor tyrosine kinases in cancer.Signal transduction and targeted therapy · 2024
    Review
  12. Review
  13. Review
  14. Review
  15. Review
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  17. Review
  18. Review
  19. Article
  20. 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.

Lucia S BorgesDepartment of Neurology, University of California, Davis, Davis, CA, United States.
David P RichmanDepartment of Neurology, University of California, Davis, Davis, CA, United States.
University of California, Davis · US

Funding

Antigen-specific treatment of myasthenia gravis: Chimeric autoantibody receptor T cells targeting autoimmune B cellsR21NS104516 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MILONE, MICHAEL C., RICHMAN, DAVID P · 2018 to 2019
$448k
NINDS NIH HHS R21 NS104516
6 · The paper itself

Abstract

Thirty to fifty percent of patients with acetylcholine receptor (AChR) antibody (Ab)-negative myasthenia gravis (MG) have Abs to muscle specific kinase (MuSK) and are referred to as having MuSK-MG. MuSK is a 100 kD single-pass post-synaptic transmembrane receptor tyrosine kinase crucial to the development and maintenance of the neuromuscular junction. The Abs in MuSK-MG are predominantly of the IgG4 immunoglobulin subclass. MuSK-MG differs from AChR-MG, in exhibiting more focal muscle involvement, including neck, shoulder, facial and bulbar-innervated muscles, as well as wasting of the involved muscles. MuSK-MG is highly associated with the HLA DR14-DQ5 haplotype and occurs predominantly in females with onset in the fourth decade of life. Some of the standard treatments of AChR-MG have been found to have limited effectiveness in MuSK-MG, including thymectomy and cholinesterase inhibitors. Therefore, current treatment involves immunosuppression, primarily by corticosteroids. In addition, patients respond especially well to B cell depletion agents, e.g., rituximab, with long-term remissions. Future treatments will likely derive from the ongoing analysis of the pathogenic mechanisms underlying this disease, including histologic and physiologic studies of the neuromuscular junction in patients as well as information derived from the development and study of animal models of the disease.

Indexed as

Adrenal Cortex HormonesAnimalsFemaleHaplotypesHLA-DR Serological SubtypesHumansImmunoglobulin GMiceMusclesMyasthenia GravisReceptor Protein-Tyrosine KinasesReceptors, CholinergicAdrenal Cortex HormonesHLA-DR14HLA-DR Serological SubtypesImmunoglobulin GMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, Cholinergicanimal modelsmuscle specific kinasemyasthenia gravisneuromuscular junctionpathogenesisreviewtreatment

Identifiers

PMID32457737
PMCPMC7225350
OpenAlexW3022783792

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.