Evidence map›Paper›PMID 38642181›Full record

ArticleMolecular biology reports2024

Tumor necrosis factor alpha induced protein 3, interleukin 10, tumor necrosis factor alpha, and interleukin 17 F genes polymorphisms in Algerian patients with rheumatoid arthritis.

D Benahmed, M Abbadi, D Zaoui, H Ait Hamoudi, W Boukouaci, S Bouguerra-Aouichat, S S Salah

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

3 citing papers in PubMed, 3 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

7 authors at 3 institutions in 1 country.

D BenahmedTeam Cellular and Molecular Physiopathology, Laboratory of Biology and physiology of organisms, Faculty of Biological Sciences, Houari Boumediene, USTHB, Algiers, Algeria. djibenahmed@yahoo.fr.
M AbbadiImmunology Department, Mustapha Bacha Teaching Hospital, Algiers, Algeria.
D ZaouiImmunology Department, Mustapha Bacha Teaching Hospital, Algiers, Algeria.
H Ait HamoudiImmunology Department, Mustapha Bacha Teaching Hospital, Algiers, Algeria.
W BoukouaciImmunology Department, Mustapha Bacha Teaching Hospital, Algiers, Algeria.
S Bouguerra-AouichatTeam Cellular and Molecular Physiopathology, Laboratory of Biology and physiology of organisms, Faculty of Biological Sciences, Houari Boumediene, USTHB, Algiers, Algeria.
S S SalahImmunology Department, Mustapha Bacha Teaching Hospital, Algiers, Algeria.
Hôpital Mustapha Pacha · DZUniversity of Algiers 3 · DZUniversity of Sciences and Technology Houari Boumediene · DZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation. Its pathogenesis involves immunological, genetic, and environmental factors. We investigate the association between Tumor Necrosis Factor α Protein 3 (TNFAIP3), Interleukin 10 (IL10), Tumor Necrosis Factor α (TNF α), and Interleukin 17 F (IL17F) polymorphisms with susceptibility to RA. METHODS AND

results191 patients with RA diagnosed according to the American College of Rheumatology (ACR)/ European League Against Rheumatism (EULAR) classification and 190 healthy subjects were recruited. Rheumatoid factor (RF), anti-citrullinated peptide antibodies (ACPA), and C-reactive protein (CRP) were measured. Genotyping of the polymorphisms was performed by real-time PCR. Analysis of the allelic frequencies of TNFAIP3 showed a positive association OR (95% CI) = 1.46 (1.01-2.09); p = 0.04, but failed to meet the criteria of significance after Bonferroni Correction. The genotypic and allelic distribution of the IL10, IL17F, and TNFα showed no significant difference when comparing the RA group with controls. Furthermore, the genotype codominant model shows a moderate positive association in the presence of ACPA (OR (95% CI) = 2.82 (1.22-6.24); p = 0.01. None of the polymorphisms studied was associated with RF and CRP production.

conclusionOur results show that there is a tendency for the AG genotype of IL10-1082 to be associated with the production of ACPA in patients with RA. None of the variants studied were associated with RA susceptibility in Algerians.

Indexed as

Arthritis, RheumatoidNorth African PeopleTumor Necrosis Factor-alphaAnti-Citrullinated Protein AntibodiesAutoantibodiesC-Reactive ProteinHumansInterleukin-10Interleukin-17Tumor Necrosis Factor alpha-Induced Protein 3Anti-Citrullinated Protein AntibodiesAutoantibodiesC-Reactive ProteinIL10 protein, humanInterleukin-10Interleukin-17Tumor Necrosis Factor-alphaTumor Necrosis Factor alpha-Induced Protein 3AutoantibodiesIL10IL17FRheumatoid arthritisTNFAIP3TNFα

Identifiers

PMID38642181
OpenAlexW4394988390

What Socratic holds

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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 Socratic graph.