Evidence map›Paper›PMID 32650733›Full record

ArticleBMC medical genetics2020

Copy number variation of IL17RA gene and its association with the ankylosing spondylitis risk in Iranian patients: a case-control study.

Hamideh Aghaei, Elham Farhadi, Maryam Akhtari, Sara Shahba, Shayan Mostafaei, Ahmadreza Jamshidi, Shiva Poursani, Mahdi Mahmoudi, Mohammad Hossein Nicknam

Open access · goldAbstract read
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In one paragraph

Article in BMC medical genetics, 2020. 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
0.6field-weighted citation impact, top 29% 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, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Mold, Mycotoxins and a Dysregulated Immune System: A Combination of Concern?International journal of molecular sciences · 2021
    Review
  4. Neuroimmune disruptions from naturally occurring levels of mycotoxins.Environmental science and pollution research international · 2021
    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

9 authors at 2 institutions in 1 country.

Hamideh AghaeiDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Elham FarhadiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Maryam AkhtariRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Sara ShahbaRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Shayan MostafaeiDepartment of Biostatistics, School of Health, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Ahmadreza JamshidiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Shiva PoursaniRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Mahdi MahmoudiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran. mahmoudim@tums.ac.ir.ORCID 0000-0002-8164-8831
Mohammad Hossein NicknamDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. mhnicknam@sina.tums.ac.ir.
Tehran University of Medical Sciences · IRKermanshah University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnkylosing spondylitis (AS) is considered as a subtype of spondyloarthritis (SpA) that mainly leads to fatigue, stiffness, spinal ankylosis, and impaired physical functions with reduced quality of life. Interleukin (IL)-17A provokes additional inflammatory mediators and recruits immune cells to the inflamed site. IL17 expression increased in various inflammatory disorders including psoriasis, rheumatoid arthritis, multiple sclerosis, crohn's disease, and ankylosing spondylitis. The current study aimed to evaluate the association of IL17RA copy number changes with the susceptibility to AS and their correlation to IL17RA expression in Iranian population.

methodsIL17RA copy number genotyping assessments were carried out in 455 AS patients and 450 healthy controls, using custom TaqMan CNV assays. TaqMan primers and probe were located in Chr.22:17109553 based on pre-designed IL17RA Copy Number Assay ID, Hs02339506_cn. mRNA expression of IL17RA was also measured by SYBR Green real-time polymerase chain reaction (PCR).

resultsA IL17RA copy number loss (< 2) was associated with AS compared to 2 copies as reference (OR:2.18, 95% CI: (1.38-3.44), P-value < 0.001) and increased the risk of AS. IL17RA mRNA expression showed a significant increase in peripheral blood mononuclear cells (PBMCs) of all AS individuals than controls. The mRNA expression level of 2 copies was significantly higher in AS patients.

conclusionsOur findings revealed that a low copy number of IL17RA might confer a susceptibility risk to AS. However, it is probably not directly involved in the regulation of IL17RA mRNA expression. Epigenetic mechanisms like DNA methylation, post-transcriptional, and -translational modifications that regulate the expression of the genes may contribute in upregulation of IL17RA mRNA expression in the loss of gene copy number condition.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseCase-Control StudiesDNA Copy Number VariationsFemaleGene Expression RegulationHumansInterleukin-17IranMaleRisk FactorsRNA, MessengerSpondylitis, AnkylosingIL17A protein, humanInterleukin-17RNA, MessengerAnkylosing spondylitisAutoimmunityCopy number variationsGene expressionIL17RA

Identifiers

PMID32650733
PMCPMC7350761
OpenAlexW3041140039

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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.