Interleukin 23 receptor gene polymorphisms and their role in the inflammatory status of rheumatoid arthritis patients in an Iranian population.
IL-23R, IL-23, IL-17A
rheumatoid arthritis
single nucleotide polymorphism
Journal
International journal of rheumatic diseases
ISSN: 1756-185X
Titre abrégé: Int J Rheum Dis
Pays: England
ID NLM: 101474930
Informations de publication
Date de publication:
Feb 2023
Feb 2023
Historique:
revised:
10
09
2022
received:
14
06
2022
accepted:
11
10
2022
pubmed:
28
10
2022
medline:
31
1
2023
entrez:
27
10
2022
Statut:
ppublish
Résumé
Several investigations have disclosed the involvement of the interleukin (IL)-23/IL-17 pathway in rheumatoid arthritis (RA) pathogenesis. Here we investigated the association of single nucleotide polymorphisms (SNPs) in the IL23 receptor (IL23R) gene with RA risk. In addition, the role of these SNPs with the inflammatory state of the patients were determined. In this case-control study, 200 RA cases and 200 healthy subjects were recruited. Using allelic discrimination real-time polymerase chain reaction, both IL23R rs10489629 and rs1004819 SNPs were genotyped. The messenger RNA (mRNA) expression levels of IL-23R, IL-23, and IL-17A were determined in peripheral blood mononuclear cells (PBMCs). The serum levels of IL-23 and IL-17A were also determined. The A allele (odds ratio [OR] = 1.52, 95% CI: 1.15-2.01; P = .0030), AA genotype (OR = 2.41, 95% CI: 1.33-4.35; P = .0035), and AG genotype (OR = 2.55, 95% CI: 1.56-4.16, P = .0002) of rs1004819 SNP was significantly associated with increased RA risk. The mRNA expression of IL-17A (fold change = 2.55, P = .00027), IL-23 (fold change = 1.62, P = .0081), and IL-23R (fold change = 1.59, P = .0077) was significantly upregulated in the PBMCs from RA patients compared to that of healthy controls. Serum levels of IL-17A (P = .00019) and IL-23 (P = .00055) was significantly higher in the RA patients compared to the controls. No significant association was detected between patient data and SNPs. The IL-23/IL-27 pathway plays a role in RA pathogenesis, but IL23R gene rs1004819 SNP might not be regulating this pathway in RA disease.
Sections du résumé
BACKGROUND
BACKGROUND
Several investigations have disclosed the involvement of the interleukin (IL)-23/IL-17 pathway in rheumatoid arthritis (RA) pathogenesis. Here we investigated the association of single nucleotide polymorphisms (SNPs) in the IL23 receptor (IL23R) gene with RA risk. In addition, the role of these SNPs with the inflammatory state of the patients were determined.
METHODS
METHODS
In this case-control study, 200 RA cases and 200 healthy subjects were recruited. Using allelic discrimination real-time polymerase chain reaction, both IL23R rs10489629 and rs1004819 SNPs were genotyped. The messenger RNA (mRNA) expression levels of IL-23R, IL-23, and IL-17A were determined in peripheral blood mononuclear cells (PBMCs). The serum levels of IL-23 and IL-17A were also determined.
RESULTS
RESULTS
The A allele (odds ratio [OR] = 1.52, 95% CI: 1.15-2.01; P = .0030), AA genotype (OR = 2.41, 95% CI: 1.33-4.35; P = .0035), and AG genotype (OR = 2.55, 95% CI: 1.56-4.16, P = .0002) of rs1004819 SNP was significantly associated with increased RA risk. The mRNA expression of IL-17A (fold change = 2.55, P = .00027), IL-23 (fold change = 1.62, P = .0081), and IL-23R (fold change = 1.59, P = .0077) was significantly upregulated in the PBMCs from RA patients compared to that of healthy controls. Serum levels of IL-17A (P = .00019) and IL-23 (P = .00055) was significantly higher in the RA patients compared to the controls. No significant association was detected between patient data and SNPs.
CONCLUSIONS
CONCLUSIONS
The IL-23/IL-27 pathway plays a role in RA pathogenesis, but IL23R gene rs1004819 SNP might not be regulating this pathway in RA disease.
Identifiants
pubmed: 36302513
doi: 10.1111/1756-185X.14479
doi:
Substances chimiques
Interleukin-17
0
Receptors, Interleukin
0
Interleukin-23
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
259-266Subventions
Organisme : Rafsanjan University of Medical Sciences
ID : IR.RUMS.REC.1400.169
Informations de copyright
© 2022 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.
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