Evidence map›Paper›PMID 33184844›Full record

ReviewClinical and experimental immunology2021

Roles of cytokines and T cells in the pathogenesis of myasthenia gravis.

A Uzawa, S Kuwabara, S Suzuki, T Imai, H Murai, Y Ozawa, M Yasuda, Y Nagane, K Utsugisawa

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07071246 (Rituximab for the Treatment of New-onset AChR-Myasthenia Gravis), which is not on this map. Cited by 86 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 3 pooled it
4.8field-weighted citation impact, top 4% 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.

NCT07071246 naactive not recruitingnot on this mapstarted 2022, after this paper: background citation

Rituximab for the Treatment of New-onset AChR-Myasthenia Gravis

TypeinterventionalSponsorTang-Du HospitalRan2022 to 2027Enrolled30ConditionsTreatmentArmsRituximab Injection
3 · Its place in the literature

Who cites it

86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Myasthenia gravis and five autoimmune diseases: a bidirectional Mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Low-dose IL-2 Ameliorates Experimental Autoimmune Myasthenia Gravis in Rats by Restoring the CD4-positive Helper T-cell Balance Via the JAK/STAT5 Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  19. Article
  20. Article

26 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

9 authors at 5 institutions in 1 country.

A UzawaDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0001-9252-1863
S KuwabaraDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
S SuzukiDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0003-4388-4574
T ImaiDepartment of Neurology, Sapporo Medical University Hospital, Sapporo, Japan.
H MuraiDepartment of Neurology, International University of Health and Welfare, Narita, Japan.
Y OzawaDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
M YasudaDepartment of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Y NaganeDepartment of Neurology, Hanamaki General Hospital, Hanamaki, Japan.
K UtsugisawaDepartment of Neurology, Hanamaki General Hospital, Hanamaki, Japan.
Chiba University · JPNational Hospital Organization Hanamaki Hospital · JPInternational University of Health and Welfare · JPKeio University · JPSapporo Medical University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is characterized by muscle weakness and fatigue caused by the presence of autoantibodies against the acetylcholine receptor (AChR) or the muscle-specific tyrosine kinase (MuSK). Activated T, B and plasma cells, as well as cytokines, play important roles in the production of pathogenic autoantibodies and the induction of inflammation at the neuromuscular junction in MG. Many studies have focused on the role of cytokines and lymphocytes in anti-AChR antibody-positive MG. Chronic inflammation mediated by T helper type 17 (Th17) cells, the promotion of autoantibody production from B cells and plasma cells by follicular Th (Tfh) cells and the activation of the immune response by dysfunction of regulatory T (T

Indexed as

AnimalsAutoantibodiesB-LymphocytesCytokinesHumansMyasthenia GravisReceptor Protein-Tyrosine KinasesReceptors, CholinergicTh17 CellsT-Lymphocytes, RegulatoryAutoantibodiesCytokinesMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, CholinergicB cellcytokinelymphocytemyasthenia gravistreatment

Identifiers

PMID33184844
PMCPMC7874834
OpenAlexW3098239695

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.