IgA1分子异常糖基化在IgA肾病中致病机理的研究
被引量：1
摘要
IgA肾病中IgA1分子铰链区O 连接糖基半乳糖基化的水平降低 ,该糖基化异常可通过多种途径引起IgA1分子在肾小球的沉积和肾小球的炎性损伤。B细胞内β1、3半乳糖基转移酶活性的缺乏可能是IgA1分子异常糖基化的原因。对该糖基化异常的深入研究将有利于进一步阐明IgA肾病的发病机制并有望对IgA肾病的治疗提供新的思路。
出处
《国外医学（泌尿系统分册）》
2004年第2期281-284,共4页
Foreign Medical Sciences(Urology and Nephrology Foreign Medical Sciences)
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