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首页> 外文期刊>Journal of genetics >Genomic dissection and prioritizing of candidate genes of QTL for regulating spontaneous arthritis on chromosome 1 in mice deficient for interleukin-1 receptor antagonist
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Genomic dissection and prioritizing of candidate genes of QTL for regulating spontaneous arthritis on chromosome 1 in mice deficient for interleukin-1 receptor antagonist

机译：白细胞介素1受体拮抗剂缺陷小鼠中染色体1的自发性关节炎的基因组解剖和QTL候选基因的优先排序

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摘要

Rheumatoid arthritis is a heterogeneous disease with clinical and biological polymorphisms. IL-1RN is a protein that binds to interleukin-1 (IL-1) receptors and inhibits the binding of IL-1-alpha and IL-1-beta. IL-1RN levels are elevated in the blood of patients with a variety of infectious, immune, and traumatic conditions. Balb/c mice deficient in IL-1ra (mouse gene of IL-1RN) develop spontaneous autoimmune arthritis while DBA/1 mice deficient in IL-1ra do not. Previously, we identified a major QTL that regulates the susceptibility to arthritis in Balb/c mice with IL-1ra deficiency. In this study, we found that the QTL may contain two peaks that are regulated by two sets of candidate genes. By haplotype analysis, the total genomic regions of candidate genes were reduced from about 19 Mbp to approximately 9 Mbp. The total number of candidate genes was reduced from 208 to 21.
机译：类风湿关节炎是一种具有临床和生物学多态性的异质性疾病。 IL-1RN是一种与白介素1（IL-1）受体结合并抑制IL-1-α和IL-1-β结合的蛋白质。患有各种传染性，免疫性和创伤性疾病的患者血液中的IL-1RN水平升高。缺乏IL-1ra（IL-1RN的小鼠基因）的Balb / c小鼠会发展为自发性自身免疫性关节炎，而缺乏IL-1ra的DBA / 1小鼠则不会。以前，我们确定了一个主要的QTL，它调节IL-1ra缺乏的Balb / c小鼠对关节炎的敏感性。在这项研究中，我们发现QTL可能包含由两组候选基因调节的两个峰。通过单倍型分析，候选基因的总基因组区域从约19 Mbp减少到约9 Mbp。候选基因的总数从208个减少到21个。

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