Evidence map›Paper›PMID 36737515›Full record

ArticleClinical rheumatology2023

Investigating the correlation of the NF-κB and FoxP3 gene expression with the plasma levels of pro- and anti-inflammatory cytokines in rheumatoid arthritis patients.

Seyed Askar Roghani, Ramin Lotfi, Bijan Soleymani, Zahra Samimi, Parisa Feizollahi, Shirin Asar, Zahra Abdan, Ali Khorasanizadeh, Mahdi Taghadosi

Abstract read
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Article in Clinical rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

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  5. Impacts of rs7528684 (-169T/C) onFrontiers in genetics · 2025
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  6. Drug design, development and therapy · 2025
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  7. Article
  8. Elevation of IL-8 secretion induced by PEDV infection via NF-κB signaling pathway.Frontiers in cellular and infection microbiology · 2024
    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 3 institutions in 1 country.

Seyed Askar RoghaniDepartment of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Ramin LotfiClinical Research Development Center, Tohid Hospital, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Bijan SoleymaniMedical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Zahra SamimiDepartment of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Parisa FeizollahiDepartment of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Shirin AsarClinical Research Development Center, Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Zahra AbdanClinical Research Development Center, Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Ali KhorasanizadehStudent Research Committee, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mahdi TaghadosiDepartment of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran. mtaghad@gmail.com.ORCID http://orcid.org/0000-0002-3516-0130
Kermanshah University of Medical Sciences · IRAhvaz Jundishapur University of Medical Sciences · IRKurdistan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRheumatoid arthritis (RA) is a chronic inflammatory systemic autoimmune disease. Cytokines regulate a wide range of inflammatory processes involved in RA pathogenesis. Anti-inflammatory cytokines (i.e., TGF-β and lL-10) and pro-inflammatory cytokines, like IL-6, were found to be potentially implicated in RA pathogenesis. Besides, NF-κB and FoxP3 are critical transcription factors regulating the inflammatory events occurring in RA patients. This study intends to assess the plasma levels of IL-6, IL-10, and TGF-β1 cytokines, as well as the expression of NF-κB and FoxP3 genes in RA patients, compared to the healthy controls.

methodsPeripheral blood was collected from 50 RA patients (25 new case and 25 under-treatment) and 25 age- and gender-matched healthy subjects. The disease activity was determined using the DAS-28 and ESR criteria. Also, plasma levels of TGF-β1, lL-10, and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) technique, and the gene expression of NF-κB and FoxP3 was evaluated using the real-time PCR method.

resultsOur results showed a significant up-regulation of Rel-A and NF-κB1, and also a down-regulation of FoxP3 gene expression in under-treatment RA patients compared to the controls (P=0.031, P=0.014, and P=0.011, respectively). Moreover, there was a significant reduction of Rel-A and FoxP3 in the under-treatment RA patients compared to new case RA patients (P=0.005 and P=0.015, respectively). Also, plasma levels of TGF-β1 were significantly increased in both the new case and under-treatment RA patients relative to controls (P<0.001).

conclusionIn conclusion, classical NF-κB (P65/P50) and FoxP3 may have significant pro- and anti-inflammatory roles in RA pathogenesis, respectively. Key Point • NF-κB (P65/P50) has a contribution to the early phase of RA.

Indexed as

Arthritis, RheumatoidNF-kappa BAnti-Inflammatory AgentsCytokinesForkhead Transcription FactorsGene ExpressionHumansInterleukin-6Transforming Growth Factor beta1Anti-Inflammatory AgentsCytokinesForkhead Transcription FactorsFOXP3 protein, humanInterleukin-6NF-kappa BTransforming Growth Factor beta1FoxP3NF-κBRegulatory T cellRheumatoid ArthritisTGF-β1

Identifiers

PMID36737515
OpenAlexW4319066297

What OpenQuestion holds

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Read underepoch 390

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.