在中国汉族人群中,Fc受体样1、3和6变异体与类风湿关节炎风险相关。

IF 2.7 4区 医学 Q2 GENETICS & HEREDITY
Yonghui Yang, Dandan Li, Chunjuan He, Linna Peng, Shishi Xing, Mei Bai, Hao Rong, Dongya Yuan, Yongjun He, Xue He, Li Wang, Tianbo Jin
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引用次数: 2

摘要

背景:类风湿性关节炎(RA)是世界上最常见的自身免疫系统疾病。近年来更多的研究表明,FCRL基因多态性与自身免疫性疾病密切相关。提示遗传因素在本病的发病机制中起重要作用。在本研究中,我们旨在探讨FCRL1 rs2050568、FCRL3 rs2317230和FCRL6 rss58240276多态性与中国汉族人群RA风险的关系。本研究招募了506例RA患者和509名健康对照者,并利用Agena MassARRAY平台成功进行了单核苷酸多态性(snp)基因分型。在调整年龄和性别后,采用优势比(ORs)和95%置信区间(95% ci)来评估这些snp多态性和RA风险。采用多因素降维(MDR)方法分析SNP-SNP相互作用。结果:这些snp的等位基因和基因型频率与RA风险无显著相关性(均p > 0.05)。按年龄和性别进行分层分析,结果证实FCRL1 rs2050568 T/T基因型增加了女性患RA的风险(p = 0.014)。FCRL3 rs2317230的G/T - T/T基因型与男性RA风险降低相关(p = 0.021)。我们还观察到FCRL6 rs58240276的C/T-T/T基因型在> 54岁组中增加了RA的风险(p = 0.016)。此外,FCRL1 rs2050568- tt、FCRL6 rss58240276 - tt和FCRL1 rs2050568- tt、FCRL3 rs2317230- tt、FCRL6 rss58240276 - tt是多位点MDR分析的最佳模型(p)。结论:我们的研究表明,FCRL1 rs2050568、FCRL3 rs2317230和FCRL6 rss58240276多态性与中国汉族人群RA易感性相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Fc receptor-like 1, 3, and 6 variants are associated with rheumatoid arthritis risk in the Chinese Han population.

Fc receptor-like 1, 3, and 6 variants are associated with rheumatoid arthritis risk in the Chinese Han population.

Fc receptor-like 1, 3, and 6 variants are associated with rheumatoid arthritis risk in the Chinese Han population.

Background: Rheumatoid arthritis (RA) is the most common autoimmune system diseases in our world. More studies in recent years have shown that FCRL gene polymorphisms is closely related to autoimmune diseases. It is suggested that genetic factors play a crucial role in the pathogenesis of this disease. In this study, we aimed to investigate the relationship between FCRL1 rs2050568, FCRL3 rs2317230 and FCRL6 rs58240276 polymorphisms and RA risk in the Chinese Han population. 506 with RA patients and 509 healthy controls were recruited in this study, and the single nucleotide polymorphisms (SNPs) was successfully genotyped using the Agena MassARRAY platform. Odds ratios (ORs) and 95% confidence intervals (95% CIs) after adjusting for age and gender were conducted to assess these SNPs polymorphisms and RA risk. The multifactor dimensionality reduction (MDR) method was conducted to analyze SNP-SNP interaction.

Results: Our results revealed that there no significant association was observed between the allele and genotype frequencies among these SNPs and RA risk (all p > 0.05). Straified analysis by age and gender, the results confirmed that FCRL1 rs2050568 T/T genotype enhanced the risk of RA in females (p = 0.014). The G/T - T/T genotype of FCRL3 rs2317230 was correlated with a decreased RA risk in males (p = 0.021). We also observed that the C/T-T/T genotype of FCRL6 rs58240276 was increased the risk of RA in the group at age >  54 years (p = 0.016). In addition, FCRL1 rs2050568-TT, FCRL6 rs58240276-TT and FCRL1 rs2050568-TT, FCRL3 rs2317230-TT, FCRL6 rs58240276-TT are the best models for multi-site MDR analysis (p < 0.05), and the two best models mentioned above and classes RA have the most significant correlation.

Conclusions: Our study demonstrated that FCRL1 rs2050568, FCRL3 rs2317230, and FCRL6 rs58240276 polymorphisms were correlated with RA susceptibility in the Chinese Han population.

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来源期刊
Genes and Environment
Genes and Environment Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
4.00
自引率
0.00%
发文量
24
审稿时长
27 weeks
期刊介绍: Genes and Environment is an open access, peer-reviewed journal that aims to accelerate communications among global scientists working in the field of genes and environment. The journal publishes articles across a broad range of topics including environmental mutagenesis and carcinogenesis, environmental genomics and epigenetics, molecular epidemiology, genetic toxicology and regulatory sciences. Topics published in the journal include, but are not limited to, mutagenesis and anti-mutagenesis in bacteria; genotoxicity in mammalian somatic cells; genotoxicity in germ cells; replication and repair; DNA damage; metabolic activation and inactivation; water and air pollution; ROS, NO and photoactivation; pharmaceuticals and anticancer agents; radiation; endocrine disrupters; indirect mutagenesis; threshold; new techniques for environmental mutagenesis studies; DNA methylation (enzymatic); structure activity relationship; chemoprevention of cancer; regulatory science. Genetic toxicology including risk evaluation for human health, validation studies on testing methods and subjects of guidelines for regulation of chemicals are also within its scope.
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