Evidence map›Paper›PMID 28540600›Full record

ReviewNeurochemical research2017

Microglial Interferon Signaling and White Matter.

Ashley McDonough, Richard V Lee, Jonathan R Weinstein

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.8field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

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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.

Ashley McDonoughDepartment of Neurology, University of Washington, Seattle, WA, 98195, USA.ORCID http://orcid.org/0000-0003-3864-9449
Richard V LeeDepartment of Neurology, University of Washington, Seattle, WA, 98195, USA.
Jonathan R WeinsteinDepartment of Neurology, University of Washington, Seattle, WA, 98195, USA. jweinste@u.washington.edu.
University of Washington · US

Funding

Microglial Interferon Signaling and Ischemic PreconditioningR01NS076620 · NINDS · UNIVERSITY OF WASHINGTON · PI WEINSTEIN, JONATHAN R · 2011 to 2015
$1.7M
Interferon Signaling in Microglia Mediates Neuroprotection in StrokeF32NS100245 · NINDS · UNIVERSITY OF WASHINGTON · PI MCDONOUGH, ASHLEY · 2017 to 2019
$198k
National Institute of Neurological Disorders and Stroke F32NS100245National Institute of Neurological Disorders and Stroke R01NS076620NINDS NIH HHS F32 NS100245NINDS NIH HHS R01 NS076620
6 · The paper itself

Abstract

Microglia, the resident immune cells of the CNS, are primary regulators of the neuroimmune response to injury. Type I interferons (IFNs), including the IFNαs and IFNβ, are key cytokines in the innate immune system. Their activity is implicated in the regulation of microglial function both during development and in response to neuroinflammation, ischemia, and neurodegeneration. Data from numerous studies in multiple sclerosis (MS) and stroke suggest that type I IFNs can modulate the microglial phenotype, influence the overall neuroimmune milieu, regulate phagocytosis, and affect blood-brain barrier integrity. All of these IFN-induced effects result in numerous downstream consequences on white matter pathology and microglial reactivity. Dysregulation of IFN signaling in mouse models with genetic deficiency in ubiquitin specific protease 18 (USP18) leads to a severe neurological phenotype and neuropathological changes that include white matter microgliosis and pro-inflammatory gene expression in dystrophic microglia. A class of genetic disorders in humans, referred to as pseudo-TORCH syndrome (PTS) for the clinical resemblance to infection-induced TORCH syndrome, also show dysregulation of IFN signaling, which leads to severe neurological developmental disease. In these disorders, the excessive activation of IFN signaling during CNS development results in a destructive interferonopathy with similar induction of microglial dysfunction as seen in USP18 deficient mice. Other recent studies implicate "microgliopathies" more broadly in neurological disorders including Alzheimer's disease (AD) and MS, suggesting that microglia are a potential therapeutic target for disease prevention and/or treatment, with interferon signaling playing a key role in regulating the microglial phenotype.

Indexed as

AnimalsHumansInterferon InducersInterferon Type IMicrogliaNervous System DiseasesPoly I-CSignal TransductionWhite MatterInterferon InducersInterferon Type IPoly I-CInterferonsMicrogliaPseudo-TORCH syndromeUsp18White matter

Identifiers

PMID28540600
PMCPMC5777301
OpenAlexW2619851622

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.