Evidence map›Paper›PMID 25135828›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

CD1d(hi)CD5+ B cells expanded by GM-CSF in vivo suppress experimental autoimmune myasthenia gravis.

Jian Rong Sheng, Songhua Quan, Betty Soliven

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  9. Article
  10. Phenotypic identification of CD19Archives of medical science : AMS · 2019
    Article
  11. Review
  12. Regulatory B cells in myasthenia gravis are differentially affected by therapies.Annals of clinical and translational neurology · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. FoxP3 Expression in Macrophages, Cancer, and B Cells-Is It Real?Clinical reviews in allergy & immunology · 2017
    Review
  17. Article
  18. Article
  19. Article
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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

3 authors at 1 institution in 1 country.

Jian Rong ShengDepartment of Neurology, University of Chicago, Chicago, IL 60637 sheng1@uchicago.edu.
Songhua QuanDepartment of Neurology, University of Chicago, Chicago, IL 60637.
Betty SolivenDepartment of Neurology, University of Chicago, Chicago, IL 60637.
University of Chicago · US

Funding

Animal models of autoimmune neuropathyR01NS064059 · NINDS · UNIVERSITY OF CHICAGO · PI SOLIVEN, BETTY C · 2010 to 2014
$1.5M
NINDS NIH HHS R01 NS064059
6 · The paper itself

Abstract

IL-10-competent subset within CD1d(hi)CD5(+) B cells, also known as B10 cells, has been shown to regulate autoimmune diseases. Whether B10 cells can prevent or suppress the development of experimental autoimmune myasthenia gravis (EAMG) has not been studied. In this study, we investigated whether low-dose GM-CSF, which suppresses EAMG, can expand B10 cells in vivo, and whether adoptive transfer of CD1d(hi)CD5(+) B cells would prevent or suppress EAMG. We found that treatment of EAMG mice with low-dose GM-CSF increased the proportion of CD1d(hi)CD5(+) B cells and B10 cells. In vitro coculture studies revealed that CD1d(hi)CD5(+) B cells altered T cell cytokine profile but did not directly inhibit T cell proliferation. In contrast, CD1d(hi)CD5(+) B cells inhibited B cell proliferation and its autoantibody production in an IL-10-dependent manner. Adoptive transfer of CD1d(hi)CD5(+) B cells to mice could prevent disease, as well as suppress EAMG after disease onset. This was associated with downregulation of mature dendritic cell markers and expansion of regulatory T cells resulting in the suppression of acetylcholine receptor-specific T cell and B cell responses. Thus, our data have provided significant insight into the mechanisms underlying the tolerogenic effects of B10 cells in EAMG. These observations suggest that in vivo or in vitro expansion of CD1d(hi)CD5(+) B cells or B10 cells may represent an effective strategy in the treatment of human myasthenia gravis.

Indexed as

AnimalsAntigens, CD1dB-LymphocytesCD5 AntigensCell ProliferationDendritic CellsDown-RegulationFemaleGranulocyte-Macrophage Colony-Stimulating FactorImmune ToleranceImmunotherapyInterleukin-10MiceMice, Inbred C57BLMyasthenia Gravis, Autoimmune, ExperimentalReceptors, CholinergicAntigens, CD1dCD1d antigen, mouseCD5 AntigensCd5 protein, mouseGranulocyte-Macrophage Colony-Stimulating FactorIL10 protein, mouseInterleukin-10Receptors, Cholinergic

Identifiers

PMID25135828
PMCPMC4167377
OpenAlexW1938633852

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.