Evidence map›Paper›PMID 26407166›Full record

ArticlePloS one2015

Disparate Effects of Mesenchymal Stem Cells in Experimental Autoimmune Encephalomyelitis and Cuprizone-Induced Demyelination.

Justin D Glenn, Matthew D Smith, Leslie A Kirby, Emily G Baxi, Katharine A Whartenby

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Justin D GlennDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Matthew D SmithDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Leslie A KirbyDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Emily G BaxiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Katharine A WhartenbyDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) are pleiotropic cells with potential therapeutic benefits for a wide range of diseases. Because of their immunomodulatory properties they have been utilized to treat autoimmune diseases such as multiple sclerosis (MS), which is characterized by demyelination. The microenvironment surrounding MSCs is thought to affect their differentiation and phenotype, which could in turn affect the efficacy. We thus sought to dissect the potential for differential impact of MSCs on central nervous system (CNS) disease in T cell mediated and non-T cell mediated settings using the MOG35-55 experimental autoimmune encephalomyelitis (EAE) and cuprizone-mediated demyelination models, respectively. As the pathogeneses of MS and EAE are thought to be mediated by IFNγ-producing (TH1) and IL-17A-producing (TH17) effector CD4+ T cells, we investigated the effect of MSCs on the development of these two key pathogenic cell groups. Although MSCs suppressed the activation and effector function of TH17 cells, they did not affect TH1 activation, but enhanced TH1 effector function and ultimately produced no effect on EAE. In the non- T cell mediated cuprizone model of demyelination, MSC administration had a positive effect, with an overall increase in myelin abundance in the brain of MSC-treated mice compared to controls. These results highlight the potential variability of MSCs as a biologic therapeutic tool in the treatment of autoimmune disease and the need for further investigation into the multifaceted functions of MSCs in diverse microenvironments and the mechanisms behind the diversity.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DeathCell ProliferationCorpus CallosumCuprizoneCytokinesDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalFemaleLymphocyte SubsetsMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinOligodendrogliaCuprizoneCytokinesMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID26407166
PMCPMC4583481
OpenAlexW2191072568

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.