Evidence map›Paper›PMID 29369915›Full record

ReviewCurrent opinion in endocrinology, diabetes, and obesity2018

Potential role of type I interferon in the pathogenic process leading to type 1 diabetes.

Natasha Qaisar, Agata Jurczyk, Jennifer P Wang

Abstract readReview
In one paragraph

Review in Current opinion in endocrinology, diabetes, and obesity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  18. Therapeutic spectrum of interferon-β in ischemic stroke.Journal of neuroscience research · 2019
    Review
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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 2 institutions in 1 country.

Natasha QaisarDepartment of Medicine.
Agata JurczykProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Jennifer P WangDepartment of Medicine.
GTx (United States) · USUniversity of Massachusetts Chan Medical School · US

Funding

Innate mechanisms for virus-induced diabetesR01AI116920 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WANG, JENNIFER P · 2016 to 2019
$2.0M
NIAID NIH HHS R01 AI116920
6 · The paper itself

Abstract

purpose of reviewUnderstanding the relationship between viral infections and the development of type 1 diabetes (T1D) is essential for T1D prevention. Virus-induced innate immune responses, specifically type I interferon (IFN-I) and the IFN gene signature, orchestrate early events of β-cell dysfunction preceding islet autoimmunity. We summarize recent advances in how IFN-I and the IFN gene signature can drive T1D development. RECENT

findingsIFN-I, particularly IFN-α, and the IFN gene signature have been detected in islets and peripheral blood of T1D patients. T1D risk genes in the IFN-I signaling pathway regulate antiviral responses in β cells driven by IFN-I and proinflammatory cytokines. Polymorphisms in these genes may cause chronic dysregulated IFN signaling in islets, characterized by hyperexpression of IFN-I, the IFN gene signature, and major histocompatibility complex class I during viral infection. Islet-cell inflammation mediated by aberrant IFN signaling drives β-cell apoptosis by initiating autoreactivity against β-cell antigens. The profound elevation in IFN-I and the IFN gene signature observed in some forms of T1D are also seen in a novel group of human autoimmune and autoinflammatory diseases called interferonopathies. SUMMARY: Despite significant advances, further studies are required to functionally dissect the mechanisms by which excessive IFN-I contributes to the evolution of autoimmunity that destroys β cells.

Indexed as

AnimalsApoptosisAutoimmunityDiabetes Mellitus, Type 1HumansImmunity, InnateInflammationInsulin-Secreting CellsInterferon Type IIslets of LangerhansSignal TransductionInterferon Type I

Identifiers

PMID29369915
PMCPMC5836805
OpenAlexW2791456551

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.