Evidence map›Paper›PMID 25917268›Full record

ReviewBritish journal of pharmacology2016

Immunoinflammatory diseases of the central nervous system - the tale of two cytokines.

M J Hofer, I L Campbell

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The application prospects of sacha inchi (Frontiers in pharmacology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. In Vitro Anti-Inflammatory Effects ofPlants (Basel, Switzerland) · 2022
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Warning SINEs: Alu elements, evolution of the human brain, and the spectrum of neurological disease.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2018
    Review
  18. Review
  19. Inflammation: maladies, models, mechanisms and molecules.British journal of pharmacology · 2016
    Article
  20. Cytokines and matrix metalloproteinases in the cerebrospinal fluid of patients with acute transverse myelitis: an outcome analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    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

2 authors at 1 institution in 1 country.

M J HoferSchool of Molecular Bioscience, University of Sydney, Sydney, Australia.
I L CampbellSchool of Molecular Bioscience, University of Sydney, Sydney, Australia.ORCID http://orcid.org/0000-0001-8681-1100
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokines are potent mediators of cellular communication that have crucial roles in the regulation of innate and adaptive immunoinflammatory responses. Clear evidence has emerged in recent years that the dysregulated production of cytokines may in itself be causative in the pathogenesis of certain immunoinflammatory disorders. Here we review current evidence for the involvement of two different cytokines, IFN-α and IL-6, as principal mediators of specific immunoinflammatory disorders of the CNS. IFN-α belongs to the type I IFN family and is causally linked to the development of inflammatory encephalopathy exemplified by the genetic disorder, Aicardi-Goutières syndrome. IL-6 belongs to the gp130 family of cytokines and is causally linked to a number of immunoinflammatory disorders of the CNS including neuromyelitis optica, idiopathic transverse myelitis and genetically linked autoinflammatory neurological disease. In addition to clinical evidence, experimental studies, particularly in genetically engineered mouse models with astrocyte-targeted, CNS-restricted production of IFN-α or IL-6 replicate many of the cardinal neuropathological features of these human cytokine-linked immunoinflammatory neurological disorders giving crucial evidence for a direct causative role of these cytokines and providing further rationale for the therapeutic targeting of these cytokines in neurological diseases where indicated.

Indexed as

AnimalsAnti-Inflammatory AgentsAutoimmune DiseasesCentral Nervous SystemHumansInflammationInterferon-alphaInterleukin-6Nervous System DiseasesAnti-Inflammatory AgentsInterferon-alphaInterleukin-6

Identifiers

PMID25917268
PMCPMC4742300
OpenAlexW2133152897

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.