Evidence map›Paper›PMID 27999109›Full record

ArticleDiabetes2017

A Critical Role for the Type I Interferon Receptor in Virus-Induced Autoimmune Diabetes in Rats.

Natasha Qaisar, Suvana Lin, Glennice Ryan, Chaoxing Yang, Sarah R Oikemus, Michael H Brodsky, Rita Bortell, John P Mordes, Jennifer P Wang

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 37 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

9 authors at 1 institution in 1 country.

Natasha QaisarDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA.
Suvana LinDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA.
Glennice RyanDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA.
Chaoxing YangDepartment of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA.
Sarah R OikemusDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA.
Michael H BrodskyDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Medical School, Worcester, MA.
Rita BortellDepartment of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA.
John P MordesDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA.
Jennifer P WangDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA jennifer.wang@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Evaluation of the role of MDA5 in virus-mediated type I diabetesR01AI092105 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WANG, JENNIFER P · 2011 to 2015
$2.0M
Innate mechanisms for virus-induced diabetesR01AI116920 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WANG, JENNIFER P · 2016 to 2019
$2.0M
Stage-specific Beta Cell Response and Biomarker Profile During Virus-induced T1DR01DK105837 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GREINER, DALE LESLIE, HARLAN, DAVID MARSHALL · 2016 to 2019
$1.5M
Innate mechanisms for virus-induced diabetesR56AI116920 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WANG, JENNIFER P · 2015 to 2015
$670k
NIAID NIH HHS R01 AI092105NIAID NIH HHS R01 AI116920NIAID NIH HHS R56 AI116920NIDDK NIH HHS R01 DK105837
6 · The paper itself

Abstract

The pathogenesis of human type 1 diabetes, characterized by immune-mediated damage of insulin-producing β-cells of pancreatic islets, may involve viral infection. Essential components of the innate immune antiviral response, including type I interferon (IFN) and IFN receptor-mediated signaling pathways, are candidates for determining susceptibility to human type 1 diabetes. Numerous aspects of human type 1 diabetes pathogenesis are recapitulated in the LEW.1WR1 rat model. Diabetes can be induced in LEW.1WR1 weanling rats challenged with virus or with the viral mimetic polyinosinic:polycytidylic acid (poly I:C). We hypothesized that disrupting the cognate type I IFN receptor (type I IFN α/β receptor [IFNAR]) to interrupt IFN signaling would prevent or delay the development of virus-induced diabetes. We generated IFNAR1 subunit-deficient LEW.1WR1 rats using CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats-associated protein 9) genome editing and confirmed functional disruption of the Ifnar1 gene. IFNAR1 deficiency significantly delayed the onset and frequency of diabetes and greatly reduced the intensity of insulitis after poly I:C treatment. The occurrence of Kilham rat virus-induced diabetes was also diminished in IFNAR1-deficient animals. These findings firmly establish that alterations in innate immunity influence the course of autoimmune diabetes and support the use of targeted strategies to limit or prevent the development of type 1 diabetes.

Indexed as

AnimalsCells, CulturedCRISPR-Cas SystemsDiabetes Mellitus, Type 1FemaleImmunity, InnateInterferon Type IMaleParvovirusRatsReal-Time Polymerase Chain ReactionReceptor, Interferon alpha-betaReverse Transcriptase Polymerase Chain ReactionInterferon Type IReceptor, Interferon alpha-beta

Identifiers

PMID27999109
PMCPMC5204313
OpenAlexW2529501131

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.