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The retention of galactose-deficient IgA1 (Gd-IgA1) in the glomerular mesangium is a hallmark of IgA nephropathy (IgAN). The immune complex formed by Gd-IgA1 binds to transferrin receptor 1 (TfR1) and deposits on mesangial cell, inducing cell proliferation, inflammatory response, matrix secretion, e...
ORGANISM(S): Homo sapiens (Human) 
2025-07-14 | PXD063709 | Pride
IgA nephropathy (IgAN) is an autoimmune disease that involves galactose-deficient IgA1 (Gal-deficient IgA1) recognized by autoantibodies to form circulating immune complexes (IgA1-IC). Some of these complexes deposit in the glomeruli and induce kidney injury. Gal-deficient IgA1 alone is not sufficie...
ORGANISM(S): Homo sapiens (Human) 
2025-11-03 | PXD055562 | Pride
IgA nephropathy (IgAN) is the most common primary glomerular disease. The characteristic pathology involves immune complexes formed by the deposition of IgA1 and underglycosylated IgA1 aggregates in the mesangial area, which may be accompanied by the deposition of IgG and/or IgM and complement compo...
ORGANISM(S): Homo sapiens 
2020-10-07 | GSE159123 | GEO
microRNA-630 regulates underglycosylated IgA1 production in the tonsils by targeting TLR4 in IgA nephropathy
Lupus IgA1 autoantibodies synergize with IgG to enhance pDC responses to RNA-containing immune complexes
Here we employ a nLC-MS/MS method to separate small amounts of purified immunoglobulins to characterize the N-glycan reportoire and site occupancy of bulk serum antibodies. Using this method, we have established, for the first time within individual donors, the N-linked glycan repotoire for bulk IgG...
ORGANISM(S): Homo sapiens (Human) 
2019-01-24 | PXD010911 | Pride
Autoantibodies to nuclear antigens are hallmarks for diagnosis of the autoimmune disease systemic lupus erythematosus (SLE) and they contribute to SLE pathogenesis. However, there remains a gap in our knowledge regarding how different isotypes of autoantibodies contribute to key disease processes, i...
ORGANISM(S): Homo sapiens 
2023-10-19 | GSE242721 | GEO
The upregulation of miR-98-5p affects the glycosylation of IgA1 through cytokines in IgA nephropathy
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