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IgA肾病发病机制-IgA1异常糖基化与免疫异常 被引量:6

Pathogenesis of IgA nephropathy: abnormal glycosylation of IgA1 and abnormal immunity
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摘要 IgA肾病(IgAN)是全球最常见的肾小球肾炎,最新研究表明,异常糖基化形成的低糖基化IgA1(Gd-IgA1)奠定了IgAN发病机制的分子基础;此外,黏膜及补体免疫异常参与IgAN发病机制的进展,其可能为IgAN的诊断、治疗指明新的方向。 IgA nephropathy(IgAN) is the most common glomerulonephritis in the world. Recent researches showed that the galactose-deficient IgA1(Gd-IgA1) laid the molecular basis of pathogenesis of IgAN. In addition,the involvement of mucosal and complement immune abnormalities in the pathogenesis of IgAN may also provide new directions for the diagnosis and treatment of IgAN.
作者 朱合 徐道亮 刘昌华 伍刚 高波 毕光宇 Zhu He Xu Daoling Liu Changhua Wu Gang Gao Bo Bi Guangyu(Central South University Xiangya School of Medicine, Changsha, Hunan 410013 Department of Nephrology, Northern Jiangsu People's Hospital, Yangzhou 225001, Jiangsu Province, China)
出处 《中华肾病研究电子杂志》 2017年第4期182-185,共4页 Chinese Journal of Kidney Disease Investigation(Electronic Edition)
关键词 IGA肾病 异常糖基化IgA1 黏膜免疫 补体系统 发病机制 IgA nephropathy Galactose-deficient-IgA1 Mucosal immunity Complement system Pathogenesis
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