Evidence map›Paper›PMID 36248775›Full record

ArticleSaudi journal of biological sciences2022

Genetic association of IL2RA, IL17RA, IL23R, and IL31RA single nucleotide polymorphisms with alopecia areata.

Mansour A Alghamdi, Laith N Al-Eitan, Hanan A Aljamal, Ayed A Shati, Mohammed A Alshehri

Open access · hybridAbstract read
In one paragraph

Article in Saudi journal of biological sciences, 2022. 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
1.1field-weighted citation impact, top 23% 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, 5 citations in OpenAlex.

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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 2 institutions in 2 countries.

Mansour A AlghamdiDepartment of Anatomy, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia.
Laith N Al-EitanDepartment of Biotechnology and Genetic Engineering, Jordan University of Science and Technology, Irbid 22110, Jordan.
Hanan A AljamalDepartment of Biotechnology and Genetic Engineering, Jordan University of Science and Technology, Irbid 22110, Jordan.
Ayed A ShatiDepartment of Child Health, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia.
Mohammed A AlshehriDepartment of Child Health, College of Medicine, King Khalid University, Abha 61421, Saudi Arabia.
King Khalid University · SAJordan University of Science and Technology · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The signalling of cytokine receptors plays a crucial role in regulating tolerance and immunity. Impaired immunological processes result in autoimmune inflammation that target the hair follicles, causing many hair disorders, mainly alopecia areata (AA). Therefore, polymorphisms in cytokine receptor genes are suggested to have a significant impact on the pathogenesis of AA, a disease with a multifactorial basis and uncertain etiology. In the present study, 152 AA patients of the Jordanian population were investigated for their genetic susceptibility to develop AA compared to 150 control subjects. Genomic DNA extraction and genotyping had conducted for IL17RA (rs879575, rs2229151, and rs4819554), IL2RA (rs3118470), IL23R (rs10889677), and IL31RA (rs161704) using the Sequenom MassARRAY® system. The allele frequency of IL17RA rs879575 is significantly higher in patients, while no statistical differences were found for IL2RA, IL23R, and IL31RA SNPs. Also, the recessive model of IL31RA rs161704 showing that AA genotype is significantly associated with AA development. To date, there is no published data regarding the association between AA and the selected genetic variants in our population. However, this study's findings assert that SNPs of IL17RA and IL31RA are linked to AA susceptibility in Jordanian patients.

Indexed as

AA, Alopecia AreataAlopecia areataAutoimmunityGenetic predispositionHair disordersIL17RA, Interleukin 17 receptor subunit alphaIL23R, Interleukin 23 receptorIL2RA, Interleukin 2 receptor subunit alphaIL31RA, Interleukin 31 receptor subunit alphaMultifactorial diseaseSNP, Single Nucleotide Polymorphism

Identifiers

PMID36248775
PMCPMC9562353
OpenAlexW4297398483

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.