Evidence map›Paper›PMID 28878127›Full record

ArticleJCI insight2017

Autoantibody-producing plasmablasts after B cell depletion identified in muscle-specific kinase myasthenia gravis.

Panos Stathopoulos, Aditya Kumar, Richard J Nowak, Kevin C O'Connor

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
5.3field-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.

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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Autoantibodies against Neurologic Antigens in Nonneurologic Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2019
    Trial
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Engaging T cells for cleanup.Frontiers in immunology · 2025
    Review
  17. Article
  18. Serological Markers of Clinical Improvement in MuSK Myasthenia Gravis.Neurology(R) neuroimmunology & neuroinflammation · 2024
    Article
  19. Review
  20. Myasthenia gravis: the future is here.The Journal of clinical investigation · 2024
    Review

1 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

4 authors at 1 institution in 1 country.

Panos Stathopoulos
Aditya Kumar
Richard J Nowak
Kevin C O'Connor
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Mechanisms of autoimmunity in myasthenia gravisR01AI114780 · NIAID · YALE UNIVERSITY · PI Kevin C O'Connor · 2016 to 2026
$4.7M
NCATS NIH HHS UL1 TR001863NIAID NIH HHS R01 AI114780
6 · The paper itself

Abstract

Myasthenia gravis (MG) is a B cell-mediated autoimmune disorder of neuromuscular transmission. Pathogenic autoantibodies to muscle-specific tyrosine kinase (MuSK) can be found in patients with MG who do not have detectable antibodies to the acetylcholine receptor (AChR). MuSK MG includes immunological and clinical features that are generally distinct from AChR MG, particularly regarding responsiveness to therapy. B cell depletion has been shown to affect a decline in serum autoantibodies and to induce sustained clinical improvement in the majority of MuSK MG patients. However, the duration of this benefit may be limited, as we observed disease relapse in MuSK MG patients who had achieved rituximab-induced remission. We investigated the mechanisms of such relapses by exploring autoantibody production in the reemerging B cell compartment. Autoantibody-expressing CD27+ B cells were observed within the reconstituted repertoire during relapse but not during remission or in controls. Using two complementary approaches, which included production of 108 unique human monoclonal recombinant immunoglobulins, we demonstrated that antibody-secreting CD27hiCD38hi B cells (plasmablasts) contribute to the production of MuSK autoantibodies during relapse. The autoantibodies displayed hallmarks of antigen-driven affinity maturation. These collective findings introduce potential mechanisms for understanding both MuSK autoantibody production and disease relapse following B cell depletion.

Indexed as

Lymphocyte DepletionAdultAgedAged, 80 and overAnimalsAutoantibodiesB-LymphocytesCohort StudiesFemaleHumansImmunologic FactorsMaleMiceMiddle AgedMyasthenia GravisReceptor Protein-Tyrosine KinasesAutoantibodiesImmunologic FactorsMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, CholinergicRituximabTumor Necrosis Factor Receptor Superfamily, Member 7Autoimmune diseasesAutoimmunityB cellsImmunologyImmunotherapy

Identifiers

PMID28878127
PMCPMC5621905
OpenAlexW2750731598

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.