Evidence map›Paper›PMID 26204230›Full record

SynthesisGenes and immunity2015

CTLA-4 as a genetic determinant in autoimmune Addison's disease.

A S B Wolff, A L Mitchell, H J Cordell, A Short, B Skinningsrud, W Ollier, K Badenhoop, G Meyer, A Falorni, O Kampe and 3 more

Open access · hybridAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Genes and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Autoimmune Thyroid Disorders in Autoimmune Addison Disease.The Journal of clinical endocrinology and metabolism · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Endocrinopathies in Inborn Errors of Immunity.Frontiers in immunology · 2021
    Review
  8. Polymorphisms in theCanine medicine and genetics · 2020
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. OncoTargets and therapy · 2018
    Article
  15. 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

13 authors at 8 institutions in 5 countries.

A S B WolffDepartment of Clinical Science, University of Bergen, Bergen, Norway.
A L MitchellInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
H J CordellInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
A ShortCentre for Integrated Genomic Medical Research, Institute of Population Health, Manchester University, Manchester, UK.
B SkinningsrudInstitute of Medical Genetics, University of Oslo, Oslo, Norway.
W OllierCentre for Integrated Genomic Medical Research, Institute of Population Health, Manchester University, Manchester, UK.
K BadenhoopDepartment of Endocrinology and Diabetes, Internal Medicine 1, Johann-Wolfgang-Goethe-University's Hospital, Frankfurt, Germany.
G MeyerDepartment of Endocrinology and Diabetes, Internal Medicine 1, Johann-Wolfgang-Goethe-University's Hospital, Frankfurt, Germany.
A FalorniDepartment of Medicine, University of Perugia, Perugia, Italy.
O KampeDepartment of Medicine, Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
D UndlienInstitute of Medical Genetics, University of Oslo, Oslo, Norway.
S H S PearceInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
E S HusebyeDepartment of Clinical Science, University of Bergen, Bergen, Norway.
Newcastle University · GBGoethe University Frankfurt · DEUniversity of Bergen · NOUniversity of Manchester · GBKarolinska Institutet · SEOslo University Hospital · NOUniversity of Oslo · NOUniversity of Perugia · IT

Funding

Medical Research Council G0701632Medical Research Council G0900001Medical Research Council G0900390Medical Research Council MR/J002526/1
6 · The paper itself

Abstract

In common with several other autoimmune diseases, autoimmune Addison's disease (AAD) is thought to be caused by a combination of deleterious susceptibility polymorphisms in several genes, together with undefined environmental factors and stochastic events. To date, the strongest genomic association with AAD has been with alleles at the HLA locus, DR3-DQ2 and DR4. The contribution of other genetic variants has been inconsistent. We have studied the association of 16 single-nucleotide polymorphisms (SNPs) within the CD28-CTLA-4-ICOS genomic locus, in a cohort comprising 691 AAD patients of Norwegian and UK origin with matched controls. We have also performed a meta-analysis including 1002 patients from European countries. The G-allele of SNP rs231775 in CTLA-4 is associated with AAD in Norwegian patients (odds ratio (OR)=1.35 (confidence interval (CI) 1.10-1.66), P=0.004), but not in UK patients. The same allele is associated with AAD in the total European population (OR=1.37 (CI 1.13-1.66), P=0.002). A three-marker haplotype, comprising PROMOTER_1661, rs231726 and rs1896286 was found to be associated with AAD in the Norwegian cohort only (OR 2.43 (CI 1.68-3.51), P=0.00013). This study points to the CTLA-4 gene as a susceptibility locus for the development of AAD, and refines its mapping within the wider genomic locus.

Indexed as

Addison DiseaseAdultCTLA-4 AntigenFemaleGenetic Association StudiesGenetic DeterminismGenetic Predisposition to DiseaseGenetic VariationHumansMaleMiddle AgedPolymorphism, Single NucleotideCTLA-4 AntigenCTLA4 protein, human

Identifiers

PMID26204230
PMCPMC4561510
OpenAlexW1859682803

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.