Evidence map›Paper›PMID 26826242›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Autoreactive T Cells from Patients with Myasthenia Gravis Are Characterized by Elevated IL-17, IFN-γ, and GM-CSF and Diminished IL-10 Production.

Yonghao Cao, Robert A Amezquita, Steven H Kleinstein, Panos Stathopoulos, Richard J Nowak, Kevin C O'Connor

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.2field-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

41 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026
    Review
  5. Article
  6. Article
  7. Targeting pathogenic Th17.1 cells via JAK-STAT3 pathway: A novel approach with tofacitinib for refractory myasthenia gravis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Skeletal Muscle and the Immune System.Advances in experimental medicine and biology · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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
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

6 authors at 1 institution in 1 country.

Yonghao CaoDepartment of Neurology, Yale School of Medicine, New Haven, CT 06511; Department of Immunobiology, Yale School of Medicine, New Haven, CT 06511; kevin.oconnor@yale.edu yonghao.cao@yale.edu.ORCID http://orcid.org/0000-0002-1350-7316
Robert A AmezquitaDepartment of Immunobiology, Yale School of Medicine, New Haven, CT 06511;
Steven H KleinsteinDepartment of Immunobiology, Yale School of Medicine, New Haven, CT 06511; Department of Pathology, Yale School of Medicine, New Haven, CT 06511; and Interdepartmental Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06511.
Panos StathopoulosDepartment of Neurology, Yale School of Medicine, New Haven, CT 06511;
Richard J NowakDepartment of Neurology, Yale School of Medicine, New Haven, CT 06511;
Kevin C O'ConnorDepartment of Neurology, Yale School of Medicine, New Haven, CT 06511; kevin.oconnor@yale.edu yonghao.cao@yale.edu.
Yale University · US

Funding

Supplement - Inflammatory Triggers in B Cell AutoimmunityU19AI056363 · NIAID · DUKE UNIVERSITY · PI ST. CLAIR, EUGENE WILLIAM · 2003 to 2017
$35.3M
Mechanisms of autoimmunity in myasthenia gravisR01AI114780 · NIAID · YALE UNIVERSITY · PI Kevin C O'Connor · 2016 to 2026
$4.7M
Mechanisms of autoantibody production in myasthenia gravisR56AI114780 · NIAID · YALE UNIVERSITY · PI O'CONNOR, KEVIN C · 2015 to 2015
$416k
NIAID NIH HHS R01 AI114780NIAID NIH HHS R01AI114780NIAID NIH HHS R56 AI114780NIAID NIH HHS U19 AI056363NIAID NIH HHS U19AI056363
6 · The paper itself

Abstract

Myasthenia gravis (MG) is a prototypical autoimmune disease that is among the few for which the target Ag and the pathogenic autoantibodies are clearly defined. The pathology of the disease is affected by autoantibodies directed toward the acetylcholine receptor (AChR). Mature, Ag-experienced B cells rely on the action of Th cells to produce these pathogenic Abs. The phenotype of the MG Ag-reactive T cell compartment is not well defined; thus, we sought to determine whether such cells exhibit both a proinflammatory and a pathogenic phenotype. A novel T cell library assay that affords multiparameter interrogation of rare Ag-reactive CD4(+) T cells was applied. Proliferation and cytokine production in response to both AChR and control Ags were measured from 3120 T cell libraries derived from 11 MG patients and paired healthy control subjects. The frequency of CCR6(+) memory T cells from MG patients proliferating in response to AChR-derived peptides was significantly higher than that of healthy control subjects. Production of both IFN-γ and IL-17, in response to AChR, was also restricted to the CCR6(+) memory T cell compartment in the MG cohort, indicating a proinflammatory phenotype. These T cells also included an elevated expression of GM-CSF and absence of IL-10 expression, indicating a proinflammatory and pathogenic phenotype. This component of the autoimmune response in MG is of particular importance when considering the durability of MG treatment strategies that eliminate B cells, because the autoreactive T cells could renew autoimmunity in the reconstituted B cell compartment with ensuing clinical manifestations.

Indexed as

AdultAgedAged, 80 and overAutoimmunityCD4-Positive T-LymphocytesCell SeparationCytokinesEnzyme-Linked Immunosorbent AssayFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon-gammaInterleukin-10Interleukin-17MaleMiddle AgedCytokinesGranulocyte-Macrophage Colony-Stimulating FactorIL10 protein, humanInterferon-gammaInterleukin-10Interleukin-17

Identifiers

PMID26826242
PMCPMC4761502
OpenAlexW2344476800

What OpenQuestion holds

Textmetadata
LicenceTDM
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.