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科学家发现自身免疫病共有易感基因

2017-02-14 黄辛、谭珊 中国科学报

今天,记者从上海交通大学医学院获悉,该院附属仁济医院沈南研究团队与美国南卡罗来纳医科大学等机构合作发现易感基因,与多种自身免疫疾病相关,为系统性红斑狼疮、类风湿性关节炎以及原发性干燥综合征等自身免疫疾病的治疗干预找到了新靶点。相关成果日前在线发表于《自然—遗传学》。



今天,记者从上海交通大学医学院获悉,该院附属仁济医院沈南研究团队与美国南卡罗来纳医科大学等机构合作发现易感基因,与多种自身免疫疾病相关,为系统性红斑狼疮、类风湿性关节炎以及原发性干燥综合征等自身免疫疾病的治疗干预找到了新靶点。相关成果日前在线发表于《自然—遗传学》。

从基因层面开展自身免疫疾病的机制研究,进而找到进行干预的有效靶点,是近年来中外风湿免疫专家所关注的研究焦点。沈南团队联合包括中科院上海生命科学院健康科学研究所、北京大学人民医院、南京医科大学、南卡罗来纳医科大学等多个研究单位,利用免疫芯片发现系统性红斑狼疮显着性相关的一个易感位点,由于该位点位于基因组非编码区域,基因表达相关性分析提示这个位点不是功能性位点。但是,该位点处于重复性多拷贝的复杂基因区域附近,无法使用高通量二代测序技术(NGS)找到与这个位点连锁的功能性致病位点,因而,研究人员始终无法锁定可以进行干预的致病位点,更无从研究致病位点的功能改变机制。



研究人员利用特异性长片段基因扩增测序的方法,在该复杂基因区域发现另一个功能性遗传易感位点,该易感位点的突变型会造成NCF1蛋白的氨基酸改变,导致NAPDH氧化酶活性氧产量减少,从而参与疾病发生发展。

“更重要的是,该位点还与类风湿关节炎和原发性干燥综合征病人的遗传易感性相关。”沈南说,这项研究在研究方法上,运用一代测序方法发现功能性致病位点,弥补了二代测序技术的漏洞,为今后发现多基因复杂遗传性疾病的功能性致病位点提供了新思路。

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