Evidence map›Paper›PMID 31676868›Full record

ArticleNature genetics2019

The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes.

Mireia Ramos-Rodríguez, Helena Raurell-Vila, Maikel L Colli, Maria Inês Alvelos, Marc Subirana-Granés, Jonàs Juan-Mateu, Richard Norris, Jean-Valery Turatsinze, Ernesto S Nakayasu, Bobbie-Jo M Webb-Robertson and 8 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 4 pooled it
19.2field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 4 syntheses or guidelines pooled it, 165 citations in OpenAlex.

  1. The role of vitamin D signalling in β cell apoptosis: a systematic review.Apoptosis : an international journal on programmed cell death · 2026
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

49 more citing papers are in PubMed but not listed here.

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

18 authors at 7 institutions in 5 countries.

Mireia Ramos-RodríguezEndocrine Regulatory Genomics Laboratory, Germans Trias i Pujol University Hospital and Research Institute, Badalona, Spain.ORCID http://orcid.org/0000-0001-8083-2445
Helena Raurell-VilaEndocrine Regulatory Genomics Laboratory, Germans Trias i Pujol University Hospital and Research Institute, Badalona, Spain.
Maikel L ColliCenter for Diabetes Research and Welbio, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Maria Inês AlvelosCenter for Diabetes Research and Welbio, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Marc Subirana-GranésEndocrine Regulatory Genomics Laboratory, Germans Trias i Pujol University Hospital and Research Institute, Badalona, Spain.
Jonàs Juan-MateuCenter for Diabetes Research and Welbio, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Richard NorrisEndocrine Regulatory Genomics Laboratory, Germans Trias i Pujol University Hospital and Research Institute, Badalona, Spain.
Jean-Valery TuratsinzeCenter for Diabetes Research and Welbio, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Ernesto S NakayasuBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA.ORCID http://orcid.org/0000-0002-4056-2695
Bobbie-Jo M Webb-RobertsonBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA.
Jamie R J InshawJDRF/Wellcome Diabetes and Inflammation Laboratory, Wellcome Centre for Human Genetics, Nuffield Department of Medicine, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Piero MarchettiDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Lorenzo PiemontiDiabetes Research Institute, San Raffaele Scientific Institute, Milan, Italy.ORCID http://orcid.org/0000-0002-2172-2198
Manel EstellerJosep Carreras Leukaemia Research Institute, Barcelona, Spain.
John A ToddJDRF/Wellcome Diabetes and Inflammation Laboratory, Wellcome Centre for Human Genetics, Nuffield Department of Medicine, NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.
Thomas O MetzBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA.
Décio L EizirikCenter for Diabetes Research and Welbio, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium.
Lorenzo PasqualiEndocrine Regulatory Genomics Laboratory, Germans Trias i Pujol University Hospital and Research Institute, Badalona, Spain. lpasquali@igtp.cat.ORCID http://orcid.org/0000-0003-2423-1826
Université Libre de Bruxelles · BEInstitut d'Investigació en Ciències de la Salut Germans Trias i Pujol · ESPacific Northwest National Laboratory · USCentre for Human Genetics · GBInstitució Catalana de Recerca i Estudis Avançats · ESJosep Carreras Leukaemia Research Institute · ESUniversity of Pisa · IT

Funding

Biomarkers Of Beta Cell Stress In Type 1 Diabetes (BetaMarker)UC4DK104166 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EIZIRIK, DECIO LAKS, EVANS-MOLINA, CARMELLA · 2014 to 2014
$2.4M
NIDDK NIH HHS UC4 DK104166
6 · The paper itself

Abstract

The early stages of type 1 diabetes (T1D) are characterized by local autoimmune inflammation and progressive loss of insulin-producing pancreatic β cells. Here we show that exposure to proinflammatory cytokines reveals a marked plasticity of the β-cell regulatory landscape. We expand the repertoire of human islet regulatory elements by mapping stimulus-responsive enhancers linked to changes in the β-cell transcriptome, proteome and three-dimensional chromatin structure. Our data indicate that the β-cell response to cytokines is mediated by the induction of new regulatory regions as well as the activation of primed regulatory elements prebound by islet-specific transcription factors. We find that T1D-associated loci are enriched with newly mapped cis-regulatory regions and identify T1D-associated variants disrupting cytokine-responsive enhancer activity in human β cells. Our study illustrates how β cells respond to a proinflammatory environment and implicate a role for stimulus response islet enhancers in T1D.

Indexed as

Gene Regulatory NetworksTranscriptomeChromatinCytokinesDiabetes Mellitus, Type 1Enhancer Elements, GeneticGene Expression RegulationGenome-Wide Association StudyHumansInsulin-Secreting CellsTranscription FactorsChromatinCytokinesTranscription Factors

Identifiers

PMID31676868
PMCPMC7040466
OpenAlexW2987280220

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.