Gene Expression of Tumor Necrosis Factor-Alpha in Etanercept-Treated Rheumatoid Arthritis Patients

Mahmood, Aseel S.; Al-Kazaz, Abdulkareem A.; Ad’hiah, Ali H.; Mayouf, Khadier K.

doi:10.4236/jbm.2017.59001

Cited by 4 publications

(9 citation statements)

References 21 publications

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“…Nevertheless, our findings disagreed with Mahmood et al (2017), andAteset al (2008) reported that TNF-α -308 is not a genetic risk factor for RA susceptibility. There are no associations also found in Pakistani and Egyptian RA patients (Rizvi et al, 2019;Elsherbini et al, 2021).…”

Section: Discussioncontrasting

confidence: 99%

Association of genetic variation in tumor necrosis factor-α gene with susceptibility to rheumatoid arthritis in southern Iraq

Jabbar¹

2023

UTJsci

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Background: Rheumatoid arthritis is the most commonly occurring systemic autoimmune disease caused by genetic, epigenetic, and environmental factors. It affects 0.5-1% of the worldwide population and increases in incidence with age. Tumor necrosis factor-?, major candidate gene in the pathogenesis of RA. Gene polymorphisms occurring in this pro-inflammatory cytokine may increase the risk of RA. This study aimed to evaluate the association between polymorphisms in TNF-? gene at location -308(rs1800629), -238(rs361525) and -376(1800750) (G/A) and RA susceptibility. The study also evaluated the effects of these polymorphisms on their corresponding gene levels in serum.Methods: This case-control study was conducted on 49 individuals (30 RA patients and 19 age- and sex-matched healthy volunteers as controls). Genomic DNA extracted from all participant blood, then amplified by PCR and genotyped by sequencing.Additionally, the serum level of TNF-? was quantified using an enzyme-linked immunosorbent assay (ELISA).Results: The results showed that thehomozygosity for the TNF-? -308 G allele significantly act as a genetic factor associated with increased RA risk (p = 0.029, OR: 4.727, 95%CI: 1.175–19.016). The A allele of -238 and -376 polymorphisms may act as a possible risk factor for RA (OR: 7.63, 95%CI:0.409-14.07; OR:6.13, 95%CI:.0.32-11.214). However, no significant differences were observed.Conclusion: The GG genotype ofTNF-? -308 SNP associated with increased rheumatoid arthritis risk.

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Section: Discussioncontrasting

confidence: 99%

Association of genetic variation in tumor necrosis factor-α gene with susceptibility to rheumatoid arthritis in southern Iraq

Jabbar¹

2023

UTJsci

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“…The tendency to not respond to etanercept was not correlated with the polymorphisms in the TNF-α promoter region at -376G/A, -806 C/T, and -1031T/C [15]. The TNF-α 308 SNP is not correlated with RA in the Iraqi population, according to another study [16].…”

Section: Resultsmentioning

confidence: 89%

“…According to a meta-analysis of earlier research, patients homozygous for the G allele respond better to anti-TNF-α therapy than those who carry the A allele at TNF-α-308 [54]. Numerous studies conducted in Iraq [9,11,14,16,18,19] on the genotype distribution for -308 G/A found that the GG genotype predominated in nearly three-quarters of the population, followed by heterozygote GA and homozygote AA. Additionally, whereas the A allele was present in a minor proportion of individuals, the G allele was detected in the majority of RA patients.…”

Section: Tnf-α Gene Polymorphism In Rheumatoid Arthritismentioning

confidence: 99%

The Association of Genetic Polymorphisms in Tumor Necrosis Factor-Alpha and Interleukins with Disease Severity or Response to Biological Therapy in Iraqi Rheumatoid Arthritis Patients: A Narrative Review

Mohammed¹,

Jamal²,

Alshamari³

2023

Al-Rafidain J Med Sci

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Background: Tumor necrosis factor-alpha (TNF-α) and interleukins play important roles in the pathogenesis of rheumatoid arthritis (RA). Genetic research has been employed to find many of the missing connections between genetic risk variations and causal genetic components. Objective: The goal of this study is to look at the genetic variations of TNF-α and interleukins in Iraqi RA patients and see how they relate to disease severity or response to biological therapy. Method: Using specific keywords, the authors conducted a systematic and comprehensive search to identify relevant Iraqi studies examining the genetic variations of TNF-α and interleukins in Iraqi RA patients and how they relate to disease severity or response to biological therapy. Results: Thirteen studies have looked at TNF-α and interleukin genetic polymorphisms in Iraqi RA patients. Only the IL-2, IL-4, IL-6, IL-17, and IL-23 receptor gene polymorphisms were explored for interleukins; however, the results of studies indicate no association between genetic polymorphism and the severity of RA. Very few researchers examine the correlation between genetic variation and TNF-α inhibitor responsiveness. Numerous studies have been conducted to investigate the genetic variations of the TNF-α promoter. The -308 G/A region in the promotor region was the most studied location.

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“…The IL4 gene expression was determined by the reverse transcription-quantitative polymerase chain reaction (RT-qPCR) technique, as previously described (12). Briefly, The GoTaq® One-Step RT-qPCR System kit (Promega, USA) was used to assess the expression.…”

Section: Gene Expression Of Il4mentioning

confidence: 99%

Gene Expression and Polymorphism of Interleukin-4 in a Sample of Iraqi Rheumatoid Arthritis Patients

Journal¹

2018

Baghdad Sci.J

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It was aimed to understand the interleukin-4 (IL-4) role in etio-pathogenesis of rheumatoid arthritis (RA). Two approaches were adopted. In the first one, a quantitative expression of IL4 gene was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and such findings were correlated with some demographic, clinical and laboratory parameters, which included gender, duration of disease, disease activity score (DAS-28), rheumatoid factors (RFs), C-reactive protein (CRP) and anti-cyclic citrullinated peptide (ACCP) antibodies. In the second approach, a single nucleotide polymorphism (SNP) of IL4 gene (rs2243250) was inspected by DNA sequencing using specific primers. Fifty-one Iraqi RA patients (22 males and 29 females) were enrolled in the study. They were under therapy, which was a single weekly subcutaneous dose of 25 mg of etanercept (Enbrel) for a period of 3-5 years. The results of gene expression (2-??Ct) revealed an increased expression of IL4 mRNA (Mean ± SEM: 8.247 ± 2.442), especially female patients compared to male patients (11.545 ± 3.928 vs. 3.537 ± 1.530; p = 0.03). The expression was also subjected to variations that were related to clinical and laboratory findings. With respect to IL4 gene SNP, allele and genotype frequencies showed no significant differences between RA patients and controls. In addition, the SNP genotypes had no effect on IL4 gene expression. In conclusion, an up-regulation of IL4 gene expression was observed in RA patients, and it was more pronounced in female than male patients by approximately four folds, while no association between the IL4 SNP alleles or genotypes and RA was observed.

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Gene Expression of Tumor Necrosis Factor-Alpha in Etanercept-Treated Rheumatoid Arthritis Patients

Cited by 4 publications

References 21 publications

Association of genetic variation in tumor necrosis factor-α gene with susceptibility to rheumatoid arthritis in southern Iraq

Association of genetic variation in tumor necrosis factor-α gene with susceptibility to rheumatoid arthritis in southern Iraq

The Association of Genetic Polymorphisms in Tumor Necrosis Factor-Alpha and Interleukins with Disease Severity or Response to Biological Therapy in Iraqi Rheumatoid Arthritis Patients: A Narrative Review

Gene Expression and Polymorphism of Interleukin-4 in a Sample of Iraqi Rheumatoid Arthritis Patients

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