Toll受体对半乳糖缺陷型IgA肾病影响机制研究进展  

Research Progress on the Mechanism of the Effect of Toll Receptor on Galactose Deficient IgA Nephropathy

作　　者：努尔加那提·努尔木哈买提 陆晨 

机构地区：[1]新疆医科大学第一附属医院肾脏病中心,新疆 乌鲁木齐

出　　处：《临床医学进展》2023年第12期20324-20328,共5页Advances in Clinical Medicine

摘　　要：IgA肾病是指肾小球系膜区以IgA或IgA沉积为主的一种原发性肾小球疾病。异常糖基化的IgA1分子,主要是循环半乳糖缺陷的IgA1,是IgA肾病系膜沉积和随后肾损伤的触发因素。近年来,发现半乳糖缺陷的IgA1在IgA肾病的发展中具有极其重要的作用。目前驱动半乳糖缺陷的IgA1产生的致病机制尚未完全阐明。已知通过Toll样受-9的先天免疫激活参与Gd-IgA1的产生。一种增殖诱导配体和IL-6也可增强IgA肾病中半乳糖缺陷的IgA1的合成。半乳糖缺陷的IgA1在临床研究中所提示其与疾病病理及进展之间的关系,以提高读者对IgA肾病发病机制的理解,本文为疾病研究提供新的思路。IgA nephropathy is a primary glomerular disease characterized by IgA or IgA deposition in the mesangial region. Abnormally glycosylated deficient IgA1 molecules, mainly circulating galactose deficient IgA1, are the trigger factors for IgA nephropathy deposition and subsequent renal injury. In recent years, it has been found that galactose deficient IgA1 plays an important role in the de-velopment of IgA nephropathy. At present, the pathogenic mechanism driving the production of galactose deficient IgA1 has not been fully elucidated. It is known that innate immune activation via Toll like receptor-9 is involved in the production of galactose deficient IgA1. A proliferation induc-ing ligand and IL-6 can also enhance the synthesis of glycosylated deficient IgA1 in IgA nephropa-thy. The relationship between glycosylated deficient IgA1 and disease pathology and progression in clinical research is suggested to improve readers’ understanding of the pathogenesis of IgA nephropathy. This paper provides new ideas for disease research.

关 键 词：IGA肾病 半乳糖缺乏型IgA1 TOLL样受体 

分 类 号：R69[医药卫生—泌尿科学]