Association of interleukin-23 receptor (IL-23R) gene polymorphisms (rs11209026, rs2201841 and rs10889677) with Egyptian rheumatoid arthritis patients

To analyse interleukin 23 receptors (IL23R) single-nucleotide polymorphism (SNPs) (rs11209026, rs2201841, and rs10889677) and to detect their association with Egyptian rheumatoid arthritis (RA) patients. The study included 120 Egyptian RA patients and 120 healthy controls that were genotyped for the...

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Bibliographic Details
Published in:Egyptian rheumatologist 2015-10, Vol.37 (4), p.159-163
Main Authors: Hamdy, Gehan, Darweesh, Hanan, Fawzy, Samar, Khattab, Enas A., Fawzy, Esmat, Sheta, Marwa
Format: Article
Language:English
Subjects:
IL-23 receptor gene polymorphism
IL-23R
Rheumatoid arthritis
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Summary:To analyse interleukin 23 receptors (IL23R) single-nucleotide polymorphism (SNPs) (rs11209026, rs2201841, and rs10889677) and to detect their association with Egyptian rheumatoid arthritis (RA) patients. The study included 120 Egyptian RA patients and 120 healthy controls that were genotyped for the three SNPs by real time/polymerase chain reaction for the first SNP and restriction fragment length polymorphism/PCR (RFLP/PCR) in the last two SNPs. The disease activity score (DAS28) was assessed in the patients. The studied patients had a mean age of 42.5±13.4years, a disease duration of 5.2±3.5years and consisted of 22 males and 98 females. Joint deformities were present in 35 and 66 patients had swollen joints. The rheumatoid factor (RF) was positive in 78.3% and the DAS28 was 3.2±1.2. Our data emphasize that the AA genotype of rs11209026 was significantly associated with RA patients compared to the controls (p=0.001). We did not find any significant association between either rs2201841 or rs10889677 and the development of RA (p=1, p=0.56 respectively). The AA allele in the 3 SNPs were remarkable frequent in those with deformities and positive RF. Our results suggest that IL23 receptor AA genotype variant of rs11209026 contributes to the aetiology of RA and may be considered a genetic marker and shared the susceptibility gene. We need to address the subgroup of patients who will benefit from the selective suppression of the IL-23 signalling which would represent new perspectives towards a personalized therapy of RA patients by further studies.
ISSN:1110-1164
2090-2433
DOI:10.1016/j.ejr.2014.12.003