Evidence map›Paper›PMID 32743495›Full record

ArticleJournal of translational autoimmunity2019

Identification and characterization of rare toll-like receptor 3 variants in patients with autoimmune Addison's disease.

Sigrid Aslaksen, Anette B Wolff, Magnus D Vigeland, Lars Breivik, Ying Sheng, Bergithe E Oftedal, Haydee Artaza, Beate Skinningsrud, Dag E Undlien, Kaja K Selmer and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. The polymorphism L412F inAutophagy · 2022
    Article
  3. Review
  4. 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

12 authors at 4 institutions in 1 country.

Sigrid AslaksenDepartment of Clinical Science, University of Bergen, Norway.
Anette B WolffDepartment of Clinical Science, University of Bergen, Norway.
Magnus D VigelandInstitute of Clinical Medicine, University of Oslo, Norway.
Lars BreivikDepartment of Clinical Science, University of Bergen, Norway.
Ying ShengDepartment of Medical Genetics, Oslo University Hospital, Norway.
Bergithe E OftedalDepartment of Clinical Science, University of Bergen, Norway.
Haydee ArtazaDepartment of Clinical Science, University of Bergen, Norway.
Beate SkinningsrudDepartment of Medical Genetics, Oslo University Hospital, Norway.
Dag E UndlienInstitute of Clinical Medicine, University of Oslo, Norway.
Kaja K SelmerDepartment of Research and Development, Division of Neuroscience, Oslo University Hospital and the University of Oslo, Norway.
Eystein S HusebyeDepartment of Clinical Science, University of Bergen, Norway.
Eirik BratlandDepartment of Clinical Science, University of Bergen, Norway.
University of Bergen · NOOslo University Hospital · NOUniversity of Oslo · NOHaukeland University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune Addison's disease (AAD) is a classic organ-specific autoimmune disease characterized by an immune-mediated attack on the adrenal cortex. As most autoimmune diseases, AAD is believed to be caused by a combination of genetic and environmental factors, and probably interactions between the two. Persistent viral infections have been suggested to play a triggering role, by invoking inflammation and autoimmune destruction. The inability of clearing infections can be due to aberrations in innate immunity, including mutations in genes involved in the recognition of conserved microbial patterns. In a whole exome sequencing study of anonymized AAD patients, we discovered several rare variants predicted to be damaging in the gene encoding Toll-like receptor 3 (TLR3). TLR3 recognizes double stranded RNAs, and is therefore a major factor in antiviral defense. We here report the occurrence and functional characterization of five rare missense variants in

Indexed as

Addison's diseaseAnti-viral immunityAutoimmunityImmunodeficiencyInnate immunityToll-like receptor 3

Identifiers

PMID32743495
PMCPMC7388336
OpenAlexW2953303094

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.