Evidence map›Paper›PMID 25084174›Full record

ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2014

Involvement of the janus kinase/signal transducer and activator of transcription signaling pathway in multiple sclerosis and the animal model of experimental autoimmune encephalomyelitis.

Etty N Benveniste, Yudong Liu, Braden C McFarland, Hongwei Qin

Open access · greenAbstract readReview
In one paragraph

Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.0field-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

52 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Review
  18. The JAK-STAT Signaling Pathway in Epilepsy.Current neuropharmacology · 2023
    Review
  19. Article
  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

4 authors at 1 institution in 1 country.

Etty N BenvenisteDepartment of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham , Birmingham, Alabama.
Yudong Liu
Braden C McFarland
Hongwei Qin
University of Alabama at Birmingham · US

Funding

Therapeutic Intervention of the JAK/STAT Pathway for NeuroinflammationR01NS057563 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2008 to 2017
$2.7M
CD40 Expression and Function in MicrogliaR01NS045290 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N. · 2003 to 2007
$1.5M
NINDS NIH HHS NS45290NINDS NIH HHS NS57563NINDS NIH HHS R01 NS057563
6 · The paper itself

Abstract

Multiple sclerosis (MS) and its animal model of experimental autoimmune encephalomyelitis (EAE) are characterized by focal inflammatory infiltrates into the central nervous system, demyelinating lesions, axonal damage, and abundant production of cytokines that activate immune cells and damage neurons and oligodendrocytes, including interleukin-12 (IL-12), IL-6, IL-17, IL-21, IL-23, granulocyte macrophage-colony stimulating factor, and interferon-gamma. The Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signaling pathway mediates the biological activities of these cytokines and is essential for the development and regulation of immune responses. Dysregulation of the JAK/STAT pathway contributes to numerous autoimmune diseases, including MS/EAE. The JAK/STAT pathway is aberrantly activated in MS/EAE because of excessive production of cytokines, loss of expression of negative regulators such as suppressors of cytokine signaling proteins, and significant enrichment of genes encoding components of the JAK/STAT pathway, including STAT3. Specific JAK/STAT inhibitors have been used in numerous preclinical models of MS and demonstrate beneficial effects on the clinical course of disease and attenuation of innate and adaptive immune responses. In addition, other drugs such as statins, glatiramer acetate, laquinimod, and fumarates have beneficial effects that involve inhibition of the JAK/STAT pathway. We conclude by discussing the feasibility of the JAK/STAT pathway as a target for neuroinflammatory diseases.

Indexed as

AnimalsAnti-Inflammatory AgentsCentral Nervous SystemCytokinesEncephalomyelitis, Autoimmune, ExperimentalEnzyme InhibitorsHumansJanus KinasesMolecular Targeted TherapyMultiple SclerosisNeurogenic InflammationOligodendrogliaSignal TransductionSTAT Transcription FactorsAnti-Inflammatory AgentsCytokinesEnzyme InhibitorsJanus KinasesSTAT Transcription Factors

Identifiers

PMID25084174
PMCPMC4118716
OpenAlexW2329190288

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.