Evidence map›Paper›PMID 26442097›Full record

ArticleFrontiers in genetics2015

Polymorphisms in Toll-like receptor genes are associated with vitiligo.

Tanel Traks, Maris Keermann, Maire Karelson, Ranno Rätsep, Ene Reimann, Helgi Silm, Eero Vasar, Sulev Kõks, Külli Kingo

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Melanogenesis Connection with Innate Immunity and Toll-Like Receptors.International journal of molecular sciences · 2020
    Review
  11. Toll-Like Receptors-2 and -4 in Graves' Disease-Key Players or Bystanders?International journal of molecular sciences · 2019
    Article
  12. 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

9 authors at 2 institutions in 1 country.

Tanel TraksDepartment of Dermatology, University of Tartu Tartu, Estonia ; Centre of Excellence for Translational Medicine, University of Tartu Tartu, Estonia.
Maris KeermannDepartment of Dermatology, University of Tartu Tartu, Estonia ; Clinic of Dermatology, Tartu University Hospital Tartu, Estonia.
Maire KarelsonDepartment of Dermatology, University of Tartu Tartu, Estonia ; Clinic of Dermatology, Tartu University Hospital Tartu, Estonia.
Ranno RätsepDepartment of Physiology, University of Tartu Tartu, Estonia.
Ene ReimannDepartment of Pathophysiology, University of Tartu Tartu, Estonia ; Department of Reproductive Biology, Estonian University of Life Sciences Tartu, Estonia.
Helgi SilmDepartment of Dermatology, University of Tartu Tartu, Estonia ; Clinic of Dermatology, Tartu University Hospital Tartu, Estonia.
Eero VasarCentre of Excellence for Translational Medicine, University of Tartu Tartu, Estonia ; Department of Physiology, University of Tartu Tartu, Estonia.
Sulev KõksCentre of Excellence for Translational Medicine, University of Tartu Tartu, Estonia ; Department of Pathophysiology, University of Tartu Tartu, Estonia ; Department of Reproductive Biology, Estonian University of Life Sciences Tartu, Estonia.
Külli KingoDepartment of Dermatology, University of Tartu Tartu, Estonia ; Clinic of Dermatology, Tartu University Hospital Tartu, Estonia.
University of Tartu · EETartu University Hospital · EE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe members of Toll-like receptor (TLR) family are responsible for recognizing various molecular patterns associated with pathogens. Their expression is not confined to immune cells and have been detected in skin cells such as keratinocytes and melanocytes. As part of a generated response to pathogens, TLRs are involved in inducing inflammatory mediators to combat these threats. It is therefore not surprising that TLRs have been implicated in inflammatory skin diseases, including atopic dermatitis and psoriasis. Likewise, as key players in autoimmunity, they have been associated with a number of autoimmune diseases. Based on this, the role of TLRs in vitiligo could be suspected, but is yet to be clearly established.

methodsIn order to conduct a genetic association analysis, 30 SNPs were selected from TLR1-TLR8 and TLR10 regions to be genotyped in Estonian case-control cohort consisting of 139 vitiligo patients and 307 healthy control individuals. The patients were further analyzed in subgroups based on sex, age of onset, occurrence of vitiligo among relatives, extent of depigmented areas, vitiligo progression activity, appearance of Köbner's phenomenon, existence of halo naevi, and incidence of spontaneous repigmentation.

resultsThe most notable finding came with SNP rs179020 situated in TLR7 gene, that was associated in entire vitiligo (Padj = 0.0065) and also several subgroup analyses. Other single marker and haplotype analyses pointed to TLR3, TLR4, and TLR10 genes.

conclusionsThis study investigated the genetic regions of nine TLR genes in relation to vitiligo susceptibility. The main results were the associations of TLR7 SNPs with vitiligo, while several other associations were obtained from the remaining TLR gene regions. This suggests that in addition to other inflammatory skin diseases, TLRs affect the development of vitiligo, thus making them interesting targets for future research.

Indexed as

autoimmunegenetic association studySNPToll-like receptorvitiligo

Identifiers

PMID26442097
PMCPMC4563240
OpenAlexW1956559859

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Registered trials

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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.