Evidence map›Paper›PMID 18776148›Full record

ReviewEndocrine reviews2008

Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis: from epidemiology to mechanisms.

Amanda Huber, Francesca Menconi, Sarah Corathers, Eric M Jacobson, Yaron Tomer

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02491567 (Study of DNA Methylation in Children and Adolescents With Autoimmune Thyroid Diseases), which is not on this map. Cited by 92 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 3 pooled it
9.9field-weighted citation impact, top 2% 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.

NCT02491567 completednot on this mapstarted 2014, after this paper: background citation

Study of DNA Methylation in Children and Adolescents With Autoimmune Thyroid Diseases

TypeobservationalSponsorAristotle University Of ThessalonikiRan2014 to 2018Enrolled110ConditionsHashimoto Thyroiditis, Graves Disease
3 · Its place in the literature

Who cites it

92 citing papers in PubMed, 3 syntheses or guidelines pooled it, 228 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Observational
  17. Genetics and epigenetics of autoimmune thyroid diseases: Translational implications.Best practice & research. Clinical endocrinology & metabolism · 2023
    Review
  18. Article
  19. Article
  20. New-onset Type 1 Diabetes after COVID-19 mRNA Vaccination.Internal medicine (Tokyo, Japan) · 2022
    Article

32 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

5 authors at 1 institution in 1 country.

Amanda HuberDivision of Endocrinology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA.
Francesca Menconi
Sarah Corathers
Eric M Jacobson
Yaron Tomer
University of Cincinnati Medical Center · US

Funding

Mapping Autoimmune Diabetes and Thyroiditis GenesR01DK067555 · NIDDK · UNIVERSITY OF CINCINNATI · PI MIHAELA STEFAN LIFSHITZ, YARON TOMER · 2005 to 2026
$5.8M
Thyroid Derived Peptide Presentation by HLA-DR in ThyroiditisR01DK073681 · NIDDK · UNIVERSITY OF CINCINNATI · PI TOMER, YARON · 2006 to 2022
$5.0M
Identifying Genes Linked to Autoimmune Thyroid DiseasesR01DK061659 · NIDDK · UNIVERSITY OF CINCINNATI · PI TOMER, YARON · 2002 to 2017
$4.1M
NIDDK NIH HHS DK067555NIDDK NIH HHS DK073681NIDDK NIH HHS DK61659NIDDK NIH HHS R01 DK061659NIDDK NIH HHS R01 DK067555NIDDK NIH HHS R01 DK073681
6 · The paper itself

Abstract

Type 1 diabetes (T1D) and autoimmune thyroid diseases (AITD) frequently occur together within families and in the same individual. The co-occurrence of T1D and AITD in the same patient is one of the variants of the autoimmune polyglandular syndrome type 3 [APS3 variant (APS3v)]. Epidemiological data point to a strong genetic influence on the shared susceptibility to T1D and AITD. Recently, significant progress has been made in our understanding of the genetic association between T1D and AITD. At least three genes have been confirmed as major joint susceptibility genes for T1D and AITD: human leukocyte antigen class II, cytotoxic T-lymphocyte antigen 4 (CTLA-4), and protein tyrosine phosphatase non-receptor type 22. Moreover, the first whole genome linkage study has been recently completed, and additional genes will soon be identified. Not unexpectedly, all the joint genes for T1D and AITD identified so far are involved in immune regulation, specifically in the presentation of antigenic peptides to T cells. One of the lessons learned from the analysis of the joint susceptibility genes for T1D and AITD is that subset analysis is a key to dissecting the etiology of complex diseases. One of the best demonstrations of the power of subset analysis is the CTLA-4 gene in T1D. Although CTLA-4 showed very weak association with T1D, when analyzed in the subset of patients with both T1D and AITD, the genetic effect of CTLA-4 was significantly stronger. Gene-gene and genetic-epigenetic interactions most likely play a role in the shared genetic susceptibility to T1D and AITD. Dissecting these mechanisms will lead to a better understanding of the etiology of T1D and AITD, as well as autoimmunity in general.

Indexed as

Diabetes Mellitus, Type 1Genetic Predisposition to DiseaseHumansThyroiditis, Autoimmune

Identifiers

PMID18776148
PMCPMC2583387
OpenAlexW2066890136

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.