Evidence map›Paper›PMID 33340282›Full record

ArticleMolecular genetics & genomic medicine2020

TH17/IL23 cytokine gene polymorphisms in bullous pemphigoid.

Pardis-Sadat Tabatabaei-Panah, Hamideh Moravvej, Sahel Aghaei, Maryam Akbari, Sakineh Rajabi, Atena Kia, Elaheh Ebrahimi, Zahra Sadaf, Alireza Atoon, Nasim Behravesh and 2 more

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Article in Molecular genetics & genomic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.9field-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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 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

12 authors at 3 institutions in 2 countries.

Pardis-Sadat Tabatabaei-PanahBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Hamideh MoravvejSkin Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Sahel AghaeiBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Maryam AkbariBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Sakineh RajabiBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Atena KiaBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Elaheh EbrahimiBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Zahra SadafBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Alireza AtoonBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Nasim BehraveshBiology Department, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Ralf J LudwigLübeck Institute of Experimental Dermatology, University of Lübeck, Lübeck, Germany.
Reza AkbarzadehSkin Research Centre, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID 0000-0001-7668-702X
Islamic Azad University South Tehran Branch · IRShahid Beheshti University of Medical Sciences · IRUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTH17/IL-23 immune axis is considered to be involved in the pathogenesis of autoimmune and chronic inflammatory diseases. Bullous pemphigoid (BP) is the most frequent autoimmune blistering disease, characterized by the presence of autoantibodies against the components of the dermal-epidermal junction. Animal studies and characterization of patient samples point toward a contribution of TH17 cells in BP pathogenesis. However, genetic polymorphisms in the genes of TH17/IL-23 cytokines have not yet been well investigated in BP.

methodsDetection of polymorphisms in IL-17A (rs2275913 and rs3819025), IL-17F (rs2397084 and rs763780), IL-17RA (rs2229151), and IL-23R (rs2201841, rs7530511, rs11209026, and rs10889677) genes were performed following the collection of blood samples and DNA extraction from BP patients and controls. Gene expression of IL-23R was determined by quantitative RT-PCR analysis.

resultsThe prevalence of IL-23R rs7530511 genotypes and alleles, as well as IL-23R rs2201841 alleles, is significantly different between the BP patients and controls. While the minor C-allele of IL-23R rs7530511 is highly present in the patients, the G-allele distribution of IL-23R rs2201841 is significantly more prevalent in the control individuals compared to the BP patients. Genotypes and alleles of other SNPs in IL-17A, IL-17F, and IL-17RA were similarly distributed in patients and controls.

conclusionsNo alteration was found in the gene expression between wild and polymorphic genotypes of IL-23R (rs2201841 and rs7530511) variations, indicating they do not contribute to altering the levels of gene expression in blood. In summary, our data show that the alleles of two SNPs in IL-23R rs2201841 and rs7530511 are associated with BP.

Indexed as

Polymorphism, Single NucleotideAgedFemaleHumansInterleukin-17MalePemphigoid, BullousReceptors, InterleukinReceptors, Interleukin-17Th17 CellsIL17A protein, humanIL17F protein, humanIL17RA protein, humanIL23R protein, humanInterleukin-17Receptors, InterleukinReceptors, Interleukin-17autoimmune diseasebullous pemphigoidgene expressiongene polymorphismTH17/IL-23 cytokines

Identifiers

PMID33340282
PMCPMC7767565
OpenAlexW3117108204

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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.