Evidence map›Paper›PMID 22099723›Full record

ArticleJournal of neuroimmunology2011

GM-CSF-induced regulatory T cells selectively inhibit anti-acetylcholine receptor-specific immune responses in experimental myasthenia gravis.

Jian Rong Sheng, Thiruppathi Muthusamy, Bellur S Prabhakar, Matthew N Meriggioli

Abstract read
In one paragraph

Article in Journal of neuroimmunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Advances in autoimmune myasthenia gravis management.Expert review of neurotherapeutics · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. GM-CSF as a therapeutic target in autoimmune diseases.Inflammation and regeneration · 2016
    Review
  18. Current Treatment, Emerging Translational Therapies, and New Therapeutic Targets for Autoimmune Myasthenia Gravis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  19. Dual Role of GM-CSF as a Pro-Inflammatory and a Regulatory Cytokine: Implications for Immune Therapy.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
    Review
  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

4 authors at 1 institution in 1 country.

Jian Rong ShengDepartment of Neurology and Rehabilitation, College of Medicine, University of Illinois at Chicago, Chicago, IL-60612, United States.
Thiruppathi Muthusamy
Bellur S Prabhakar
Matthew N Meriggioli
University of Illinois Chicago · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR029879 · NCRR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAZZONE, THEODORE · 2009 to 2011
$11.0M
Therapeutic treatment of EAT by inducing dendritic cellR01AI058190 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PRABHAKAR, BELLUR S · 2006 to 2010
$1.8M
Immunoregulation of Experimental Autoimmune Myasthenia GravisK08NS058800 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MERIGGIOLI, MATTHEW NICHOLAS · 2007 to 2011
$886k
NCRR NIH HHS UL1 RR029879NCRR NIH HHS UL1RR029879NIAID NIH HHS R01 AI 058190NIAID NIH HHS R01 AI058190NINDS NIH HHS K08 NS058800NINDS NIH HHS K08NS058800
6 · The paper itself

Abstract

We and others have demonstrated the ability of granulocyte-macrophage colony-stimulating factor (GM-CSF) to suppress autoimmunity by increasing the number of CD4(+)CD25(+) regulatory T cells (Tregs). In the current study, we have explored the critical role of induced antigen specific Tregs in the therapeutic effects of GM-CSF in murine experimental autoimmune myasthenia gravis (EAMG). Specifically, we show that Tregs from GM-CSF treated EAMG mice (GM-CSF/AChR-induced-Tregs) adoptively transferred into animals with EAMG suppressed clinical disease more potently than equal numbers of Tregs from either GM-CSF untreated EAMG mice or healthy mice treated with GM-CSF. In addition, GM-CSF/AChR-induced-Tregs selectively suppressed antigen specific T cell proliferation induced by AChR relative to that induced by an irrelevant self antigen, (thyroglobulin) and failed to significantly alter T cell proliferation in response to an exogenous antigen (ovalbumin). These results are consistent with the hypothesized mechanism of action of GM-CSF involving the mobilization of tolerogenic dendritic cell precursors which, upon antigen (AChR) capture, suppress the anti-AChR immune response through the induction/expansion of AChR-specific Tregs.

Indexed as

Antibody SpecificityAdoptive TransferAnimalsAutoantibodiesCell ProliferationCholinergic AntagonistsDendritic CellsFemaleGranulocyte-Macrophage Colony-Stimulating FactorImmune ToleranceMiceMice, Inbred C57BLMyasthenia Gravis, Autoimmune, ExperimentalReceptors, CholinergicStem CellsT-Lymphocytes, RegulatoryAutoantibodiesCholinergic AntagonistsGranulocyte-Macrophage Colony-Stimulating FactorReceptors, Cholinergic

Identifiers

PMID22099723
PMCPMC3234297
OpenAlexW2020019417

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.