类风湿关节炎患者白细胞介素-10和Foxp3作为关键生物标志物的基因表达

Q4 Biochemistry, Genetics and Molecular Biology Biomedicine (India) Pub Date : 2023-08-30 DOI:10.51248/.v43i4.3107
Rakad M. Kh Al-Jumaily, Iman I. AL-Sheakli, Haidar J. Muhammed, Bahaa Abdullah Lafttah Al-Rubaii
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引用次数: 0

摘要

叉头盒P3 (FOXP3)和白细胞介素-10 (IL-10)是控制Treg细胞活性的关键调节因子,在维持免疫耐受和减少自身免疫反应中起着至关重要的作用。本研究的目的是探讨FOXP3和IL-10基因表达水平升高作为类风湿关节炎(RA)患者诊断指标的潜在作用。材料与方法:采用定量聚合酶链反应(qPCR)检测伊拉克类风湿性关节炎患者全血样本中FOXP3和IL-10转录本的表达水平。一组健康的对照组也被纳入研究。结果:在伊拉克类风湿性关节炎患者的血液样本中,与健康对照组相比,FOXP3基因表达水平有统计学意义的降低(p0.01), IL-10表达水平有统计学意义的升高(p0.01)。结论:伊拉克类风湿关节炎患者可能受益于FOXP3和IL-10基因表达检测。IL-10和FOXP3过表达促进T细胞和免疫系统的免疫反应性。
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Gene expression of Interleukin-10 and Foxp3 as critical biomarkers in rheumatoid arthritis patients
Introduction and Aim: Forkhead box P3 (FOXP3) and interleukin-10 (IL-10) are the key regulators controlling the activity of Treg cells, which are crucial for maintaining immune tolerance and reducing autoimmune reactions. The objective of this study was to investigate the potential utility of elevated levels of FOXP3 and IL-10 gene expression as a diagnostic indicator in patients with rheumatoid arthritis (RA). Materials and Methods: The study used quantitative polymerase chain reaction (qPCR) to examine the expression levels of FOXP3 and IL-10 transcripts in whole blood samples from Iraqi patients with rheumatoid arthritis. A group of healthy control subjects were also included in the study. Results: In blood samples taken from Iraqi patients diagnosed with rheumatoid arthritis, a statistically significant decrease (P 0.01) in the expression levels of the FOXP3 gene and a statistically significant elevation (P 0.01) of IL-10 expression were seen in contrast to the healthy control group. Conclusion: Rheumatoid arthritis patients in Iraq may benefit from FOXP3 and IL-10 gene expression tests. IL-10 and FOXP3 overexpression promotes T cell and immune system immunoreactivity.
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来源期刊
Biomedicine (India)
Biomedicine (India) Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
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