Several studies have reported genetic polymorphisms at the IL-23/IL-17 axis linked to rheumatoid arthritis (RA) in many populations. We aimed to investigate the association of IL-17A rs2275913 and IL-23R rs11209026 polymorphisms with susceptibility to RA and, disease clinical features and the serum level of IL-17A in Egyptian patients. This case-control study included 94 RA cases and 74 controls. TaqMan genotyping assays were used for detection of gene polymorphism and the enzyme-linked immunosorbent assay was used to quantify IL-17A serum level. There was significant difference between RA patients and controls in genotypic distribution and allelic frequency of IL-17A rs 2275913 (p < 0.0001). The GG genotype had 7 times higher risk for RA development (OR=7.04: 95% CI 2.11:23.46, p value= 0.001). Also, GG genotype was associated with higher level of serum IL-17 A compared to GA and AA genotypes (p < 0.0001). Moreover, patients carrying the GG genotype had higher disease activity score 28 (DAS28) score (4.99±0.84) compared to patients with GA (2.73±0.52, p < 0.0001) and patients with AA genotypes (2.67±0.41, p < 0.0001). Genotypic distribution of IL-23R rs11209026 was significantly different between RA patients and controls (p < 0.0001), but there was no difference between the allelic frequency in both groups (p=0.08). IL-23R rs11209026 SNP was not a risk for RA development. However, DAS28 was lower in AA genotype than AG and GG genotypes (p=0.002, p=0.009 respectively). The mean serum IL-17A level was higher among the RA patients (39.07±10.47 pg./ mL) compared to controls (15.23±1.88 pg/ mL; p < 0.0001). Also, there was a positive correlation between IL-17A serum level and DAS28 score (Spearman r = 0.42; p value < 0.0001). We concluded that the variant IL-17A (rs2275913) genotype could be a risk factor for RA in our population and IL-17A may play a crucial role in the development and pathogenesis of RA.
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Biochem Genet
October 2024
ImmGen EvSys Lab, Department of Biotechnology, Berhampur University, Bhanja Bihar, Berhampur, Odisha, 760007, India.
The etiology of Rheumatoid Arthritis (RA) development remained unclear, and several factors, such as environmental, genetic, and immune system dysfunction, have been attributed to the susceptibility. Interleukin 23 (IL23) induces expansion of the Th17 cells through the IL-23 receptor (IL-23R) and believes in playing a major role in RA pathogenesis. Various genetic mutants in the IL23R gene (rs10489629, rs1343151, rs2201841, rs7517847, rs1004819, rs10889677, rs11209026, rs7530511) have been associated with the susceptibility RA, but results are contradictories.
View Article and Find Full Text PDFEgypt J Immunol
July 2023
Department of Medical Microbiology and Immunology, Faculty of Medicine, Sohag University, Sohag, Egypt.
Several studies have reported genetic polymorphisms at the IL-23/IL-17 axis linked to rheumatoid arthritis (RA) in many populations. We aimed to investigate the association of IL-17A rs2275913 and IL-23R rs11209026 polymorphisms with susceptibility to RA and, disease clinical features and the serum level of IL-17A in Egyptian patients. This case-control study included 94 RA cases and 74 controls.
View Article and Find Full Text PDFEgypt J Immunol
April 2023
Department of Medical Microbiology and Immunology, Faculty of Medicine, Sohag University, Sohag, Egypt.
Severe COVID-19 disease was linked to a severe proinflammatory response and cytokine storm interleukin 17 (IL-17) is one of these cytokines, was associated with severe acute lung injury and multiorgan dysfunction. Single nucleotide polymorphisms (SNPs) in genes coding IL-17 can affect level of IL-17 hence its role in diseases. Also, SNPs in IL-23 R which control IL-23 is the main activator of IL-17 production.
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June 2022
Department of Dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, China.
Psoriasis is a common immune-mediated inflammatory skin disease. Although biological agents have achieved good clinical efficacy in the treatment of moderate-to-severe psoriasis, the phenomenon of secondary non-response (SNR) has been gradually recognized. SNR refers to the gradual decline of efficacy after the patient achieves clinical remission with biological agents such as TNF-α biologics.
View Article and Find Full Text PDFJ Clin Med
December 2021
Department of Biochemistry, "Iuliu Hațieganu" University of Medicine and Pharmacy Cluj-Napoca, 400000 Cluj-Napoca, Romania.
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