作者: Steven N. Emancipator , Jiri Mestecky , Michael E. Lamm
DOI: 10.1016/B978-012491543-5/50096-6
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摘要: IgA nephropathy (IgAN) is caused by the accumulation of IgA-immune complexes (IC) in glomeruli. The enzymes that assemble glycan side chains on various glycoproteins and glycolipids are highly sensitive to external stimuli, including cytokines. Some Th2 cytokines dominate cellular immune responses Peyer's patches elicit increased production also promote hypogalactosylation both O -linked N glycans, at least vitro. In patients with IgAN, synthesis (increased ks and/or ks') represents humoral mucosal antigens. within single samples IC from individual IgAN not only polyclonal but polyspecific, is, includes antibodies bind several antigens, complexed antigens often originate distinct sources. Furthermore, implicated associated portals entry, temporal associations between antigen entry (via dietary exposure infection) exacerbations nephritis well established. Thus, glomerular deposits represent combined synthesized large part (or mucosally derived) plasma cells.