Evidence map›Paper›PMID 32547535›Full record

ReviewFrontiers in immunology2020

Autoimmune Pathology in Myasthenia Gravis Disease Subtypes Is Governed by Divergent Mechanisms of Immunopathology.

Miriam L Fichtner, Ruoyi Jiang, Aoibh Bourke, Richard J Nowak, Kevin C O'Connor

Registry-linked trialOpen access · goldAbstract readReview
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. It is linked to trial NCT05301153 (Expression Levels of Interleukin 37 and Its Correlation With Autoantibodies and Disease Severity in Myasthenia Gravis Patients), which is not on this map. Cited by 91 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 6 pooled it
5.7field-weighted citation impact, top 3% 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.

NCT05301153 unknown statusnot on this mapstarted 2022, after this paper: background citation

Expression Levels of Interleukin 37 and Its Correlation With Autoantibodies and Disease Severity in Myasthenia Gravis Patients

TypeobservationalSponsorAssiut UniversityRan2022 to 2024Enrolled82ConditionsMyasthenia GravisArmsreal time PCR , ELISA
3 · Its place in the literature

Who cites it

91 citing papers in PubMed, 6 syntheses or guidelines pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Rituximab for myasthenia gravis.The Cochrane database of systematic reviews · 2025
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Anti-acetylcholine receptor antibody overshoot following efgartigimod in myasthenia gravis: Two case reports with literature review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  15. Article
  16. Italian recommendations for the diagnosis and treatment of myasthenia gravis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  17. Article
  18. Review
  19. Telitacicept as a New Therapeutic Avenue for Generalized Myasthenia Gravis and Thymoma-Associated Myasthenia Gravis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  20. Article

31 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 2 institutions in 2 countries.

Miriam L FichtnerDepartment of Neurology, School of Medicine, Yale University, New Haven, CT, United States.
Ruoyi JiangDepartment of Immunobiology, School of Medicine, Yale University, New Haven, CT, United States.
Aoibh BourkeTrinity Hall, University of Cambridge, Cambridge, United Kingdom.
Richard J NowakDepartment of Neurology, School of Medicine, Yale University, New Haven, CT, United States.
Kevin C O'ConnorDepartment of Neurology, School of Medicine, Yale University, New Haven, CT, United States.
Yale University · USUniversity of Cambridge · GB

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Rare Disease Network for Myasthenia GravisU54NS115054 · NINDS · GEORGE WASHINGTON UNIVERSITY · PI HENRY J KAMINSKI · 2019 to 2026
$11.9M
Mechanisms of autoimmunity in myasthenia gravisR01AI114780 · NIAID · YALE UNIVERSITY · PI Kevin C O'Connor · 2016 to 2026
$4.7M
Novel Approaches for Investigating the Pathology of Myasthenia Gravis AutoantibodiesR21AI142198 · NIAID · YALE UNIVERSITY · PI O'CONNOR, KEVIN C · 2019 to 2020
$395k
NIAID NIH HHS R01 AI114780NIAID NIH HHS R21 AI142198NIGMS NIH HHS T32 GM007205NINDS NIH HHS U54 NS115054
6 · The paper itself

Abstract

Myasthenia gravis (MG) is a prototypical autoantibody mediated disease. The autoantibodies in MG target structures within the neuromuscular junction (NMJ), thus affecting neuromuscular transmission. The major disease subtypes of autoimmune MG are defined by their antigenic target. The most common target of pathogenic autoantibodies in MG is the nicotinic acetylcholine receptor (AChR), followed by muscle-specific kinase (MuSK) and lipoprotein receptor-related protein 4 (LRP4). MG patients present with similar symptoms independent of the underlying subtype of disease, while the immunopathology is remarkably distinct. Here we highlight these distinct immune mechanisms that describe both the B cell- and autoantibody-mediated pathogenesis by comparing AChR and MuSK MG subtypes. In our discussion of the AChR subtype, we focus on the role of long-lived plasma cells in the production of pathogenic autoantibodies, the IgG1 subclass mediated pathology, and contributions of complement. The similarities underlying the immunopathology of AChR MG and neuromyelitis optica (NMO) are highlighted. In contrast, MuSK MG is caused by autoantibody production by short-lived plasmablasts. MuSK MG autoantibodies are mainly of the IgG4 subclass which can undergo Fab-arm exchange (FAE), a process unique to this subclass. In FAE IgG4, molecules can dissociate into two halves and recombine with other half IgG4 molecules resulting in bispecific antibodies. Similarities between MuSK MG and other IgG4-mediated autoimmune diseases, including pemphigus vulgaris (PV) and chronic inflammatory demyelinating polyneuropathy (CIDP), are highlighted. Finally, the immunological distinctions are emphasized through presentation of biological therapeutics that provide clinical benefit depending on the MG disease subtype.

Indexed as

AnimalsAntibodies, BispecificAutoantibodiesB-LymphocytesHumansImmunoglobulin GLDL-Receptor Related ProteinsMiceMyasthenia GravisPemphigusPolyradiculoneuropathy, Chronic Inflammatory DemyelinatingReceptor Protein-Tyrosine KinasesReceptors, CholinergicReceptors, NicotinicAntibodies, BispecificAutoantibodiesCHRNG protein, humanImmunoglobulin GLDL-Receptor Related ProteinsLRP4 protein, humanMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, CholinergicReceptors, NicotinicAChRautoantibodiesautoimmunityB cellsB lymphocytesimmunopathologyMuSKmyasthenia gravis

Identifiers

PMID32547535
PMCPMC7274207
OpenAlexW3031008534

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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 Socratic graph.