Evidence map›Paper›PMID 21653838›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Overexpression of the dominant-negative form of interferon regulatory factor 1 in oligodendrocytes protects against experimental autoimmune encephalomyelitis.

Zhihua Ren, Yan Wang, Duan Tao, David Liebenson, Thomas Liggett, Rajendra Goswami, Robert Clarke, Dusan Stefoski, Roumen Balabanov

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. NF-κB Activation Accounts for the Cytoprotective Effects of PERK Activation on Oligodendrocytes during EAE.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Deletion of interferon-regulatory factor-1 results in cognitive impairment.Hypertension research : official journal of the Japanese Society of Hypertension · 2018
    Article
  17. Review
  18. Article
  19. Review
  20. 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

9 authors at 2 institutions in 1 country.

Zhihua RenRush University Medical Center, Department of Neurological Sciences, Multiple Sclerosis Center, Chicago, Illinois 60612, USA.
Yan Wang
Duan Tao
David Liebenson
Thomas Liggett
Rajendra Goswami
Robert Clarke
Dusan Stefoski
Roumen Balabanov
Rush University Medical Center · USGeorgetown University Medical Center · US

Funding

Oligodendrocyte response to interferon-gammaK08NS050409 · NINDS · UNIVERSITY OF CHICAGO · PI BALABANOV, ROUMEN DELTCHEV · 2005 to 2009
$729k
NINDS NIH HHS K08 NS5040901
6 · The paper itself

Abstract

Interferon regulatory factor 1 (IRF-1) is a transcription factor that has been implicated in the pathogenesis of the human autoimmune demyelinating disease multiple sclerosis (MS) and in its animal model, experimental autoimmune encephalomyelitis (EAE). The goal of the present study was to directly examine the role of IRF-1 in oligodendrocyte injury and inflammatory demyelination. For the purpose of this study, we generated a transgenic mouse line (CNP/dnIRF-1) that overexpresses the dominant-negative form of IRF-1 (dnIRF1) specifically in oligodendrocytes. CNP/dnIRF-1 mice exhibited no phenotypic abnormalities but displayed suppressed IRF-1 signaling in oligodendrocytes. The major finding of our study was that the CNP/dnIRF-1 mice, compared with the wild-type mice, were protected against EAE, a phenomenon associated with significant reduction of inflammatory demyelination and with oligodendrocyte and axonal preservation. The observed protection was related to suppressed IRF-1 signaling and impaired expression of immune and proapoptotic genes in oligodendrocytes. No significant differences in the peripheral immune responses between the wild-type and the CNP/dnIRF-1 mice were identified throughout the experiments. This study indicates that IRF-1 plays a critical role in the pathogenesis of EAE by mediating oligodendrocyte response to inflammation and injury. It also suggests that oligodendrocytes are actively involved in the neuroimmune network, and that exploring oligodendrocyte-related pathogenic mechanisms, in addition to the conventional immune-based ones, may have important therapeutic implications in MS.

Indexed as

AnimalsDemyelinating DiseasesElectrophoresisEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryImmunohistochemistryInflammationInterferon Regulatory Factor-1MiceMice, TransgenicOligodendrogliaReverse Transcriptase Polymerase Chain ReactionInterferon Regulatory Factor-1

Identifiers

PMID21653838
PMCPMC3770885
OpenAlexW2151702579

What OpenQuestion holds

Textmetadata
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.