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中华肾病研究电子杂志 ›› 2017, Vol. 06 ›› Issue (04) : 182 -185. doi: 10.3877/cma.j.issn.2095-3216.2017.04.010

所属专题: 文献

综述

IgA肾病发病机制-IgA1异常糖基化与免疫异常
朱合1, 徐道亮1,(), 刘昌华2, 伍刚2, 高波2, 毕光宇2   
  1. 1. 410013 湖南长沙,中南大学湘雅医学院;225001 江苏省扬州市苏北人民医院肾内科
    2. 225001 江苏省扬州市苏北人民医院肾内科
  • 收稿日期:2017-01-21 出版日期:2017-08-28
  • 通信作者: 徐道亮

Pathogenesis of IgA nephropathy: abnormal glycosylation of IgA1 and abnormal immunity

He Zhu1, Daoling Xu1,(), Changhua Liu2, Gang Wu2, Bo Gao2, Guangyu Bi2   

  1. 1. Central South University Xiangya School of Medicine, Changsha, Hunan 410013; Department of Nephrology, Northern Jiangsu People′s Hospital, Yangzhou 225001, Jiangsu Province; China
    2. Department of Nephrology, Northern Jiangsu People′s Hospital, Yangzhou 225001, Jiangsu Province; China
  • Received:2017-01-21 Published:2017-08-28
  • Corresponding author: Daoling Xu
  • About author:
    Corresponding author: Xu Daoliang, Email:
引用本文:

朱合, 徐道亮, 刘昌华, 伍刚, 高波, 毕光宇. IgA肾病发病机制-IgA1异常糖基化与免疫异常[J]. 中华肾病研究电子杂志, 2017, 06(04): 182-185.

He Zhu, Daoling Xu, Changhua Liu, Gang Wu, Bo Gao, Guangyu Bi. Pathogenesis of IgA nephropathy: abnormal glycosylation of IgA1 and abnormal immunity[J]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2017, 06(04): 182-185.

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.

图1 异常糖基化及黏膜免疫异常所致IgA肾病机制图示
[1]
Moriyama T, Tanaka K, Iwasaki C, et al. Prognosis in IgA nephropathy: 30-year analysis of 1,012 patients at a single center in Japan [J]. PLoS One, 2014, 9(3): e91756.
[2]
Yanagawa H, Suzuki H, Suzuki Y, et al. A panel of serum biomarkers differentiates IgA nephropathy from other renal diseases [J]. PLoS One, 2014, 9(5): e98081.
[3]
Robert T, Berthelot L, Cambier A, et al. Molecular insights into the pathogenesis of IgA nephropathy [J]. Trends Mol Med, 2015, 21(12): 762-775.
[4]
谢静远,陈楠.IgA肾病的临床进展[J]. 中国实用内科杂志,2011, 31(2): 90-93.
[5]
Suzuki H, Raska M, Yamada K, et al. Cytokines alter IgA1 O-glycosylation by dysregulating C1GalT1 and ST6GalNAc-II enzymes[J]. J Biol Chem, 2014, 289(8): 5330-5339.
[6]
Suzuki H, Moldoveanu Z, Hall S, et al. IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1 [J]. J Clin Invest,2008, 118(2): 629-639.
[7]
秦伟,杨立川,谭淳予,等.外周血b淋巴细胞β1,3半乳糖基转移酶及其伴侣蛋白核酸表达和IgA肾病的关系[J]. 中华肾脏病杂志,2007, 23(10): 677-678.
[8]
Inoue T, Sugiyama H, Kitagawa M, et al. Abnormalities of glycogenes in tonsillar lymphocytes in IgA nephropathy [J]. Adv Otorhinolaryngol, 2011, 72: 71-74.
[9]
王金泉.IgA肾病的遗传易感性和黏膜免疫应答异常[J]. 医学研究生学报,2016, 29(2): 120-125.
[10]
Meng H, Ohtake H, Ishida A, et al. IgA production and tonsillar focal infection in IgA nephropathy [J]. J Clin Exp Hematop, 2012, 52(3): 161-170.
[11]
伍刚,彭佑铭,徐道亮,等.腭扁桃体及外周血中记忆B细胞在IgA肾病临床进展中的异常表达[J]. 北京大学学报(医学版), 2015, 47(5): 749-753.
[12]
Vergano L, Loiacono E, Albera R, et al. Can tonsillectomy modify the innate and adaptive immunity pathways involved in IgA nephropathy [J]. J Nephrol, 2015, 28(1): 51-58.
[13]
Kiryluk K, Novak J. The genetics and immunobiology of IgA nephropathy [J]. J Clin Invest, 2014, 124(6): 2325-2332.
[14]
Coppo R. The intestine-renal connection in IgA nephropathy [J]. Nephrol Dial Transplant, 2015, 30(3): 360-366.
[15]
Vieira SM, Pagovich OE, Kriegel MA. Diet, microbiota and autoimmune diseases[J]. Lupus, 2014, 23(6): 518-526.
[16]
Qin W, Zhong X, Fan JM, et al. External suppression causes the low expression of the Cosmc gene in IgA nephropathy [J]. Nephrol Dial Transplant, 2008, 23(5): 1608-1614.
[17]
Coppo R, Camilla R, Amore A, et al. Toll-like receptor 4 expression is increased in circulating mononuclear cells of patients with immunoglobulin A nephropathy [J]. Clin Exp Immunol, 2010, 159(1): 73-81.
[18]
Skerka C, Chen Q, Fremeaux-Bacchi V, et al. Complement factor H related proteins (CFHRs) [J]. Mol Immunol, 2013, 56(3): 170-180.
[19]
Wyatt RJ, Julian BA. IgA nephropathy [J]. N Engl J Med, 2013, 368(25): 2402-2414.
[20]
Gharavi AG, Kiryluk K, Choi M, et al. Genome-wide association study identifies susceptibility loci for IgA nephropathy [J]. Nat Genet, 2011, 43(4): 321-327.
[21]
Zhu L, Zhai YL, Wang FM, et al. Variants in complement factor H and complement factor H-related protein genes, CFHR3 and CFHR1, affect complement activation in IgA nephropathy [J]. J Am Soc Nephrol, 2015, 26(5): 1195-1204.
[22]
Maillard N, Wyatt RJ, Julian BA, et al. Current understanding of the role of complement in IgA nephropathy [J]. J Am Soc Nephrol, 2015, 26(7): 1503-1512.
[23]
Xie J, Kiryluk K, Li Y, et al. Fine mapping implicates a deletion of CFHR1 and CFHR3 in protection from IgA nephropathy in Han Chinese[J]. J Am Soc Nephrol, 2016, 27(10): 3187-3194.
[24]
Fritsche LG, Lauer N, Hartmann A, et al. An imbalance of human complement regulatory proteins CFHR1, CFHR3 and factor H influences risk for age-related macular degeneration (AMD) [J]. Hum Mol Genet, 2010, 19(23): 4694-4704.
[25]
Ohsawa I, Ishii M, Ohi H, et al. Pathological scenario with the mannose-binding lectin in patients with IgA nephropathy [J]. J Biomed Biotechnol, 2012, 2012: 476739.
[26]
Jozsi M, Zipfel PF. Factor H family and human diseases [J]. Trends Immunol, 2008, 29(8): 380-387.
[27]
Peng Q, Li K, Smyth LA, et al. C3a and C5a promote renal ischemia-reperfusion injury [J]. J Am Soc Nephrol, 2012, 23(9): 1474-1485.
[28]
Ohsawa I, Ishii M, Ohi H, et al. Pathological scenario with the mannose-binding lectin in patients with IgA nephropathy [J]. J Biomed Biotechnol, 2012, 2012: 476739.
[29]
Peng Q, Li K, Lesley A, et al.C3a and C5a promote renal ischemia-reperfusion injury [J]. J Am Soc Nephrol, 2012, 23(9): 1173-1181.
[30]
Engelke C, Wiese AV, Schmudde I, et al. Distinct roles of the anaphylatoxins C3a and C5a in dendritic cell-mediated allergic asthma [J]. J Immunol, 2014, 193(11): 5387-5401.
[31]
Hashimoto A, Suzuki Y, Suzuki H, et al. Determination of severity of murine IgA nephropathy by glomerular complement activation by aberrantly glycosylated IgA and immune complexes [J]. Am J Pathol,2012, 181(4): 1338-1347.
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