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肿瘤坏死因子 α 诱导蛋白 3、白细胞介素 10、肿瘤坏死因子 α 和白细胞介素 17F 基因多态性与阿尔及利亚类风湿关节炎患者。

Tumor necrosis factor alpha induced protein 3, interleukin 10, tumor necrosis factor alpha, and interleukin 17 F genes polymorphisms in Algerian patients with rheumatoid arthritis.

机构信息

Team Cellular and Molecular Physiopathology, Laboratory of Biology and physiology of organisms, Faculty of Biological Sciences, Houari Boumediene, USTHB, Algiers, Algeria.

Immunology Department, Mustapha Bacha Teaching Hospital, Algiers, Algeria.

出版信息

Mol Biol Rep. 2024 Apr 20;51(1):545. doi: 10.1007/s11033-024-09525-2.

DOI:10.1007/s11033-024-09525-2
PMID:38642181
Abstract

BACKGROUND

Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation. Its pathogenesis involves immunological, genetic, and environmental factors. We investigate the association between Tumor Necrosis Factor α Protein 3 (TNFAIP3), Interleukin 10 (IL10), Tumor Necrosis Factor α (TNF α), and Interleukin 17 F (IL17F) polymorphisms with susceptibility to RA.

METHODS AND RESULTS

191 patients with RA diagnosed according to the American College of Rheumatology (ACR)/ European League Against Rheumatism (EULAR) classification and 190 healthy subjects were recruited. Rheumatoid factor (RF), anti-citrullinated peptide antibodies (ACPA), and C-reactive protein (CRP) were measured. Genotyping of the polymorphisms was performed by real-time PCR. Analysis of the allelic frequencies of TNFAIP3 showed a positive association OR (95% CI) = 1.46 (1.01-2.09); p = 0.04, but failed to meet the criteria of significance after Bonferroni Correction. The genotypic and allelic distribution of the IL10, IL17F, and TNFα showed no significant difference when comparing the RA group with controls. Furthermore, the genotype codominant model shows a moderate positive association in the presence of ACPA (OR (95% CI) = 2.82 (1.22-6.24); p = 0.01. None of the polymorphisms studied was associated with RF and CRP production.

CONCLUSION

Our results show that there is a tendency for the AG genotype of IL10-1082 to be associated with the production of ACPA in patients with RA. None of the variants studied were associated with RA susceptibility in Algerians.

摘要

背景

类风湿关节炎(RA)是一种慢性炎症性的系统性自身免疫性疾病。其发病机制涉及免疫、遗传和环境因素。我们研究了肿瘤坏死因子α蛋白 3(TNFAIP3)、白细胞介素 10(IL10)、肿瘤坏死因子α(TNFα)和白细胞介素 17F(IL17F)多态性与 RA 易感性之间的关系。

方法和结果

我们招募了 191 名根据美国风湿病学会(ACR)/欧洲抗风湿病联盟(EULAR)分类标准诊断的 RA 患者和 190 名健康对照者。测量了类风湿因子(RF)、抗瓜氨酸肽抗体(ACPA)和 C 反应蛋白(CRP)。通过实时 PCR 进行多态性的基因分型。对 TNFAIP3 的等位基因频率进行分析,发现阳性关联 OR(95%CI)=1.46(1.01-2.09);p=0.04,但经 Bonferroni 校正后未达到显著性标准。在 RA 组与对照组比较时,IL10、IL17F 和 TNFα 的基因型和等位基因分布没有显著差异。此外,在存在 ACPA 的情况下,基因型显性模型显示出中度正关联(OR(95%CI)=2.82(1.22-6.24);p=0.01)。研究的多态性与 RF 和 CRP 的产生均无相关性。

结论

我们的结果表明,在 RA 患者中,IL10-1082 的 AG 基因型与 ACPA 的产生有一定的相关性。在所研究的变体中,没有一个与阿尔及利亚人的 RA 易感性相关。

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Tumor necrosis factor-α -308 polymorphism in North Indian rheumatoid arthritis patients and association with mRNA and serum TNF-α.肿瘤坏死因子-α-308 多态性与北印度类风湿关节炎患者 mRNA 和血清 TNF-α 的关系。
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