title: The genetics and immunobiology of IgA nephropathy.
abstract: IgA nephropathy (IgAN) represents the leading cause of kidney failure among East Asian populations and the most frequent form of primary glomerulonephritis among Europeans. Patients with IgAN develop characteristic IgA1-containing immune complexes that deposit in the glomerular mesangium, producing progressive kidney injury. Recent studies define IgAN as an autoimmune trait of complex architecture with a strong genetic determination. This Review summarizes new insights into the role of the O-glycosylation pathway, anti-glycan immune response, mucosal immunity, antigen processing and presentation, and the alternative complement pathway in the pathogenesis of IgAN.
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Kiryluk
authors.forename: Jan
authors.initials: J
authors.lastname: Novak
mesh_terms: D000595:Amino Acid Sequence; D017951:Antigen Presentation; D000936:Antigen-Antibody Complex / Q000097:blood / Q000378:metabolism; D003170:Complement Pathway, Alternative; D055106:Genome-Wide Association Study; D005922:Glomerulonephritis, IGA / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D006031:Glycosylation; D006801:Humans; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000097:blood / Q000737:chemistry / Q000235:genetics; D008957:Models, Genetic; D018448:Models, Immunological; D008969:Molecular Sequence Data; D015394:Molecular Structure
chemical_list: D000936:Antigen-Antibody Complex; D007070:Immunoglobulin A