Evidence map›Paper›PMID 26397019›Full record

ReviewCurrent opinion in neurobiology2016

Fine-tuning of type I IFN-signaling in microglia--implications for homeostasis, CNS autoimmunity and interferonopathies.

Tobias Goldmann, Thomas Blank, Marco Prinz

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-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

29 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
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  8. Article
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  11. Review
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  14. Modulation of cGAS-STING signaling by PPARα in a mouse model of ischemia-induced retinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Review
  16. Functional immune cell-astrocyte interactions.The Journal of experimental medicine · 2021
    Review
  17. Review
  18. Article
  19. Microglial responses to peripheral type 1 interferon.Journal of neuroinflammation · 2020
    Article
  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

3 authors at 1 institution in 1 country.

Tobias GoldmannInstitute of Neuropathology, University of Freiburg, Germany.
Thomas BlankInstitute of Neuropathology, University of Freiburg, Germany.
Marco PrinzInstitute of Neuropathology, University of Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, University of Freiburg, Germany. Electronic address: marco.prinz@uniklinik-freiburg.de.
University of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons (IFN) are pleiotropic cytokines originally described as molecules used for communication between cells to trigger the protective defenses against viral infections. Upon activation, type I IFN can be produced locally in the central nervous system (CNS) from a number of different cell types including microglia, the CNS-resident macrophages. Increased type I IFN production and signaling in microglia are critically important to limit viral infection and disease progression in multiple sclerosis. However, recent findings suggest that even baseline levels of constitutive IFN expression and secretion are important for homeostasis of the CNS. In fact, in the absence of viral particles chronic elevation of IFN I may be tremendously harmful for the CNS, as assumed for patients suffering from Aicardi-Goutières syndrome, Cree encephalitis or other type I interferonopathies. The highly diverse nature of type I IFN for brain homeostasis during health and disease will be discussed in this report.

Indexed as

Autoimmune Diseases of the Nervous SystemAutoimmunityCentral Nervous SystemHomeostasisHumansInterferon Type IMicrogliaMultiple SclerosisMyelin SheathNervous System MalformationsPhagocytosisSignal TransductionInterferon Type I

Identifiers

PMID26397019
PMCPMC7126514
OpenAlexW1708550902

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.