Evidence map›Paper›PMID 24417588›Full record

ArticleBrain pathology (Zurich, Switzerland)2014

Protective and detrimental roles for regulatory T cells in a viral model for multiple sclerosis.

Nicholas E Martinez, Fridrik Karlsson, Fumitaka Sato, Eiichiro Kawai, Seiichi Omura, Alireza Minagar, Matthew B Grisham, Ikuo Tsunoda

Open access · bronzeAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. The Safety ofViruses · 2026
    Article
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  18. Cytotoxic CD8Brain pathology (Zurich, Switzerland) · 2018
    Article
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  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

8 authors at 2 institutions in 1 country.

Nicholas E MartinezDepartment of Microbiology and Immunology, Center for Molecular and Tumor Virology, Louisiana State University Health Sciences Center, Shreveport, LA.
Fridrik Karlsson
Fumitaka Sato
Eiichiro Kawai
Seiichi Omura
Alireza Minagar
Matthew B Grisham
Ikuo Tsunoda
Louisiana State University Health Sciences Center Shreveport · USTexas Tech University · US

Funding

RECRUITMENT YEAR FOR PI#5P20RR018724 · NCRR · LOUISIANA STATE UNIV HSC SHREVEPORT · PI TSUNODA, IKUO · 2003 to 2011
$16.1M
COBRE Center for Molecular and Tumor VirologyP30GM110703 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI SAPP, MARTIN · 2014 to 2018
$4.8M
COBRE Center for Molecular and Tumor VirologyP20GM103433 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI O'CALLAGHAN, DENNIS JOHN · 2012 to 2012
$1.9M
Axonal degeneration can trigger demyelinating diseaseR21NS059724 · NINDS · UNIVERSITY OF UTAH · PI TSUNODA, IKUO · 2008 to 2009
$357k
NCRR NIH HHS P20 RR018724NIGMS NIH HHS 8P20 GM103433NIGMS NIH HHS P20 GM103433NIGMS NIH HHS P30 GM110703NINDS NIH HHS R21 NS059724NINDS NIH HHS R21NS059724
6 · The paper itself

Abstract

Multiple sclerosis (MS) has been proposed to be an immune-mediated disease in the central nervous system (CNS) that can be triggered by virus infections. In Theiler's murine encephalomyelitis virus (TMEV) infection, during the first week (acute stage), mice develop polioencephalomyelitis. After 3 weeks (chronic stage), mice develop immune-mediated demyelination with virus persistence, which has been used as a viral model for MS. Regulatory T cells (Tregs) can suppress inflammation, and have been suggested to be protective in immune-mediated diseases, including MS. However, in virus-induced inflammatory demyelination, although Tregs can suppress inflammation, preventing immune-mediated pathology, Tregs may also suppress antiviral immune responses, leading to more active viral replication and/or persistence. To determine the role and potential translational usage of Tregs in MS, we treated TMEV-infected mice with ex vivo generated induced Tregs (iTregs) on day 0 (early) or during the chronic stage (therapeutic). Early treatment worsened clinical signs during acute disease. The exacerbation of acute disease was associated with increased virus titers and decreased immune cell recruitment in the CNS. Therapeutic iTreg treatment reduced inflammatory demyelination during chronic disease. Immunologically, iTreg treatment increased interleukin-10 production from B cells, CD4(+) T cells and dendritic cells, which may contribute to the decreased CNS inflammation.

Indexed as

AnimalsBrainCardiovirus InfectionsEncephalitisFemaleMiceMice, Inbred C57BLMultiple SclerosisPoliomyelitisSpinal CordTheilovirusT-Lymphocytes, RegulatoryautoimmunityCNS demyelinating diseaseimmunologyinflammationPicornaviridae infectionsregulatory T lymphocyte

Identifiers

PMID24417588
PMCPMC4097993
OpenAlexW1956239516

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.