Evidence map›Paper›PMID 24378287›Full record

ArticleJournal of autoimmunity2014

Characterization of CD4 and CD8 T cell responses in MuSK myasthenia gravis.

J S Yi, A Guidon, S Sparks, R Osborne, V C Juel, J M Massey, D B Sanders, K J Weinhold, J T Guptill

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. FOSL1-mediated LINC01566 negatively regulates CD4Journal of neuroinflammation · 2024
    Article
  4. Review
  5. An angel or a devil? Current view on the role of CD8Journal of translational medicine · 2024
    Review
  6. Article
  7. Myasthenia gravis associated with muscle-specific kinase antibodies in a patient treated with interleukin-17 inhibitor.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Antibody Therapies in Autoimmune Neuromuscular Junction Disorders: Approach to Myasthenic Crisis and Chronic Management.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. CD4Frontiers in immunology · 2020
    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

9 authors at 2 institutions in 1 country.

J S YiDivision of Surgical Sciences, Department of Surgery, Duke University Medical Center, 204 SORF (Bldg. 41), 915 S. LaSalle Street, Box 2926, Durham, NC 27710, USA.
A GuidonNeuromuscular Division, Department of Neurology, Duke University Medical Center, DUMC Box 3403, Durham, NC 27710, USA.
S SparksDivision of Surgical Sciences, Department of Surgery, Duke University Medical Center, 204 SORF (Bldg. 41), 915 S. LaSalle Street, Box 2926, Durham, NC 27710, USA.
R OsborneDivision of Surgical Sciences, Department of Surgery, Duke University Medical Center, 204 SORF (Bldg. 41), 915 S. LaSalle Street, Box 2926, Durham, NC 27710, USA.
V C JuelNeuromuscular Division, Department of Neurology, Duke University Medical Center, DUMC Box 3403, Durham, NC 27710, USA.
J M MasseyNeuromuscular Division, Department of Neurology, Duke University Medical Center, DUMC Box 3403, Durham, NC 27710, USA.
D B SandersNeuromuscular Division, Department of Neurology, Duke University Medical Center, DUMC Box 3403, Durham, NC 27710, USA.
K J WeinholdDivision of Surgical Sciences, Department of Surgery, Duke University Medical Center, 204 SORF (Bldg. 41), 915 S. LaSalle Street, Box 2926, Durham, NC 27710, USA.
J T GuptillNeuromuscular Division, Department of Neurology, Duke University Medical Center, DUMC Box 3403, Durham, NC 27710, USA. Electronic address: jeffrey.guptill@duke.edu.
Duke Medical Center · USDuke University Hospital · US

Funding

Social and Behavioral Sciences CoreP30AI064518 · NIAID · DUKE UNIVERSITY · PI Nwora Lance Okeke · 2005 to 2026
$50.5M
Pilot Project for the DTMI CRA ProgramUL1RR024128 · NCRR · DUKE UNIVERSITY · PI CALIFF, ROBERT M · 2006 to 2010
$48.1M
NCRR NIH HHS UL1 RR024128NCRR NIH HHS UL1RR024128NIAID NIH HHS P30 AI064518NIAID NIH HHS P30 AI 64518
6 · The paper itself

Abstract

Muscle specific tyrosine kinase myasthenia gravis (MuSK MG) is a form of autoimmune MG that predominantly affects women and has unique clinical features, including prominent bulbar weakness, muscle atrophy, and excellent response to therapeutic plasma exchange. Patients with MuSK MG have predominantly IgG4 autoantibodies directed against MuSK on the postsynaptic muscle membrane. Lymphocyte functionality has not been reported in this condition. The goal of this study was to characterize T cell responses in patients with MuSK MG. Intracellular production of IFN-gamma, TNF-alpha, IL-2, IL-17, and IL-21 by CD4+ and CD8+ T cells was measured by polychromatic flow cytometry in peripheral blood samples from 11 Musk MG patients and 10 healthy controls. Only one MuSK MG patient was not receiving immunosuppressive therapy. Regulatory T cells (Treg) were also included in our analysis to determine if changes in T cell function were due to altered Treg frequencies. CD8+ T cells from MuSK MG patients had higher frequencies of polyfunctional responses than controls, and CD4+ T cells had higher IL-2, TNF-alpha, and IL-17. MuSK MG patients had a higher percentage of CD4+ T cells producing combinations of IFN-gamma/IL-2/TNF-gamma, TNF-alpha/IL-2, and IFN-gamma/TNF-alpha. Interestingly, Treg numbers and CD39 expression were not different from control values. MuSK MG patients had increased frequencies of Th1 and Th17 cytokines and were primed for polyfunctional proinflammatory responses that cannot be explained by a defect in CD39 expression or Treg number.

Indexed as

AdultAgedCD8-Positive T-LymphocytesCell SeparationCytokinesFemaleFlow CytometryHumansImmunoglobulin GImmunophenotypingMiddle AgedMyasthenia GravisReceptor Protein-Tyrosine KinasesReceptors, CholinergicSex FactorsTh17 CellsCytokinesImmunoglobulin GMUSK protein, humanReceptor Protein-Tyrosine KinasesReceptors, CholinergicAutoimmunityHumanMuSK proteinMyasthenia gravisRegulatoryT-lymphocytes

Identifiers

PMID24378287
PMCPMC4230445
OpenAlexW2053967648

What OpenQuestion holds

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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.