Glycosylation of IgA1 and pathogenesis of IgA nephropathy

被引:117
作者
Novak, Jan [1 ]
Julian, Bruce A. [1 ]
Mestecky, Jiri [1 ]
Renfrow, Matthew B. [1 ]
机构
[1] Univ Alabama Birmingham, Dept Microbiol, Birmingham, AL 35294 USA
基金
美国国家卫生研究院;
关键词
IgA nephropathy; IgA1; O-glycans; High-resolution mass spectrometry; Measangial cells; HUMAN MESANGIAL CELLS; ELECTRON-CAPTURE DISSOCIATION; FLIGHT MASS-SPECTROMETRY; HUMAN SERUM IGA1; O-LINKED OLIGOSACCHARIDES; HENOCH-SCHONLEIN PURPURA; GALACTOSE-DEFICIENT IGA1; HUMAN COLONIC MUCIN; IGA1-CONTAINING IMMUNE-COMPLEXES; IMMUNOGLOBULIN-A NEPHROPATHY;
D O I
10.1007/s00281-012-0306-z
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
IgA nephropathy, described in 1968 as IgA-IgG immune-complex disease, is an autoimmune disease. Galactose-deficient IgA1 is recognized by unique autoantibodies, resulting in the formation of pathogenic immune complexes that ultimately induce glomerular injury. Thus, formation of the galactose-deficient IgA1-containing immune complexes is a critical factor in the pathogenesis of IgA nephropathy. Studies of molecular defects of IgA1 can define new biomarkers specific for IgA nephropathy that can be developed into clinical assays to aid in the diagnosis, assessment of prognosis, and monitoring of disease progression.
引用
收藏
页码:365 / 382
页数:18
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