Evidence map›Paper›PMID 26061776›Full record

ArticleeLife2015

Differential cell autonomous responses determine the outcome of coxsackievirus infections in murine pancreatic α and β cells.

Laura Marroqui, Miguel Lopes, Reinaldo S dos Santos, Fabio A Grieco, Merja Roivainen, Sarah J Richardson, Noel G Morgan, Anne Op de Beeck, Decio L Eizirik

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
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  4. From bats to humans: uncoveringbioRxiv : the preprint server for biology · 2026
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  15. The pathogenesis of coronavirus-19 disease.Journal of biomedical science · 2022
    Review
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  18. 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

9 authors at 3 institutions in 3 countries.

Laura MarroquiULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Miguel LopesULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Reinaldo S dos SantosULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Fabio A GriecoULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Merja RoivainenNational Institute for Health and Welfare, Helsinki, Finland.
Sarah J RichardsonInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, Exeter, United Kingdom.
Noel G MorganInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, Exeter, United Kingdom.
Anne Op de BeeckULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Decio L EizirikULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Université Libre de Bruxelles · BEUniversity of Exeter · GBFinnish Institute for Health and Welfare · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease caused by loss of pancreatic β cells via apoptosis while neighboring α cells are preserved. Viral infections by coxsackieviruses (CVB) may contribute to trigger autoimmunity in T1D. Cellular permissiveness to viral infection is modulated by innate antiviral responses, which vary among different cell types. We presently describe that global gene expression is similar in cytokine-treated and virus-infected human islet cells, with up-regulation of gene networks involved in cell autonomous immune responses. Comparison between the responses of rat pancreatic α and β cells to infection by CVB5 and 4 indicate that α cells trigger a more efficient antiviral response than β cells, including higher basal and induced expression of STAT1-regulated genes, and are thus better able to clear viral infections than β cells. These differences may explain why pancreatic β cells, but not α cells, are targeted by an autoimmune response during T1D.

Indexed as

Immunity, InnateAnimalsCoxsackievirus InfectionsGene Expression ProfilingGene Expression RegulationGlucagon-Secreting CellsHumansInsulin-Secreting CellsRats, Wistarapoptosiscell biologycytokinesdiabetes mellitushumanimmunologymousepancreatic alpha cellpancreatic beta cellratvirus and diabetesviruses

Identifiers

PMID26061776
PMCPMC4480275
OpenAlexW2110765003

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.