Evidence map›Paper›PMID 30888520›Full record

ReviewCurrent diabetes reports2019

Genetic Mechanisms Highlight Shared Pathways for the Pathogenesis of Polygenic Type 1 Diabetes and Monogenic Autoimmune Diabetes.

Matthew B Johnson, Karen Cerosaletti, Sarah E Flanagan, Jane H Buckner

Open access · hybridAbstract readReview
In one paragraph

Review in Current diabetes reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.6field-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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Case Report: A novel mutation inFrontiers in endocrinology · 2023
    Article
  6. Clinical and experimental treatment of type 1 diabetes.Clinical and experimental immunology · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. HLA Polymorphisms and Food Allergy Predisposition.Journal of pediatric genetics · 2020
    Review
  13. Review
  14. Emerging Roles of Exosomes in T1DM.Frontiers in immunology · 2020
    Review
  15. Article
  16. Review
  17. Article
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

4 authors at 2 institutions in 2 countries.

Matthew B JohnsonInstitute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, UK.
Karen CerosalettiTranslational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA.
Sarah E FlanaganInstitute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, UK. S.Flanagan@exeter.ac.uk.
Jane H BucknerTranslational Research Program, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA.
University of Exeter · GBVirginia Mason Medical Center · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
An integrated strategy to define the functional and synergistic impact of T1D causal variantsDP3DK111802 · NIDDK · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2016 to 2016
$4.4M
NIDDK NIH HHS DP3 DK111802NIDDK NIH HHS P30 DK017047Wellcome TrustWellcome Trust 105636/Z/14/Z
6 · The paper itself

Abstract

purpose of reviewTo highlight pathways important for the development of autoimmune diabetes by investigating shared mechanisms of disease in polygenic and monogenic diabetes. RECENT

findingsGenome-wide association studies have identified 57 genetic risk loci for type 1 diabetes. Progress has been made in unravelling the mechanistic effects of some of these variants, providing key insights into the pathogenesis of type 1 diabetes. Seven monogenic disorders have also been described where diabetes features as part of an autoimmune syndrome. Studying these genes in relation to polygenic risk loci provides a unique opportunity to dissect pathways important for the development of immune-mediated diabetes. Monogenic autoimmune diabetes can result from the dysregulation of multiple pathways suggesting that small effects on many immune processes are required to drive the autoimmune attack on pancreatic beta cells in polygenic type 1 diabetes. A breakdown in central and peripheral immune tolerance is a common theme in the genetic mechanisms of both monogenic and polygenic disease which highlights the importance of these checkpoints in the development and treatment of islet autoimmunity.

Indexed as

Autoimmune DiseasesDiabetes Mellitus, Type 1AutoimmunityGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansAutoimmunityImmune toleranceMonogenic diabetesPolygenic risk

Identifiers

PMID30888520
PMCPMC6424922
OpenAlexW2924948389

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.