Evidence map›Paper›PMID 26656450›Full record

ArticleGenes and immunity

Variation in the CTLA4 3'UTR has phenotypic consequences for autoreactive T cells and associates with genetic risk for type 1 diabetes.

V M de Jong, A Zaldumbide, A R van der Slik, S Laban, B P C Koeleman, B O Roep

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Association ofCurrent issues in molecular biology · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Genetic aspects of type 1 diabetes.Annals of pediatric endocrinology & metabolism · 2019
    Article
  8. Article
  9. Message from the new Editors-in-Chief.Genes and immunity · 2019
    Article
  10. Review
  11. Article
  12. Genetics of type 1 diabetes.Pediatric diabetes · 2018
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Tremelimumab-Induced Graves Hyperthyroidism.European thyroid journal · 2017
    Article
  18. Article
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

V M de JongDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
A ZaldumbideDepartment of Molecular Cell Biology, Leiden University Medical Center, Leiden, The Netherlands.
A R van der SlikDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
S LabanDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
B P C KoelemanDepartment of Medical Genetics, University Medical Center Utrecht, Utrecht, The Netherlands.
B O RoepDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
Leiden University Medical Center · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytotoxic T-lymphocyte-associated protein 4 (CTLA4) is a protein receptor that downregulates the immune system. CTLA4 gene variants associate with various autoimmune diseases, including type 1 diabetes. Fine mapping of the genetic risk has shown that the genomic region near CTLA4 marked by the single-nucleotide polymorphism (SNP) CT60A/G (rs3087243) acts as a susceptibility factor. Yet, the functional basis for the increased susceptibility conferred by rs3087243 remains unclear. We demonstrate that the length of the dinucleotide (AT)n repeat within the CTLA4 3' untranslated region (3'UTR) strongly associates with the risk of SNP CT60A/G (P<6.5 × 10(-72)). Genomic (AT)n repeat length inversely correlated with CTLA4 messenger RNA (mRNA) and protein levels in islet autoreactive T-cell lines. Transfer of a long (AT)n element into T cells lead to a reduction of mRNA compared to a short (AT)n element. Thus, this study provides evidence for a role of the CTLA4 3'UTR (AT)n repeat in the increased genetic risk for islet autoimmunity associated with the CTLA4 locus.

Indexed as

3' Untranslated RegionsDinucleotide RepeatsGenetic Predisposition to DiseaseCTLA-4 AntigenDiabetes Mellitus, Type 1HumansRNA Processing, Post-TranscriptionalT-Lymphocytes3' Untranslated RegionsCTLA-4 AntigenCTLA4 protein, human

Identifiers

PMID26656450
OpenAlexW2267121625

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.