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IgA肾病发病机制及其进展 被引量:1

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摘要 近十几年来,通过分子生物学及基因遗传学方法的研究显示,糖基化缺陷的IgA1(Gd-IgA1)是原发性IgA肾病(IgAN)的本质基础并可被遗传,涉及免疫蛋白酶体(ips)及Toll-Like受体(TLR)等的免疫调节异常在IgAN中起重要作用.基因多态性分析揭示C1GALT1及T6GALNAC2基因多态性与国人IgAN易感性相关,MHC区6p、HLA区含有欧州人群IgAN的易感性等位基因.近来发现miRNAs在IgAN进展中起作用.环境因素(如病毒感染)可能在IgAN发病机制中起着“二次打击”的作用.
出处 《国际泌尿系统杂志》 2014年第4期593-595,共3页 International Journal of Urology and Nephrology
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