ArticleProceedings of the National Academy of Sciences of the United States of America1988
Circulating complexes containing IgA and fibronectin in patients with primary IgA nephropathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026Review
- Pathogenesis of IgA Nephropathy: Current Understanding and Implications for Development of Disease-Specific Treatment.Journal of clinical medicine · 2021Review
- Article
- Binding Truths: Atypical Anti-Glomerular Basement Membrane Disease Mediated by IgA Anti-Glomerular Basement Membrane Antibodies Targeting the α1 Chain of Type IV Collagen.Kidney international reports · 2019Article
- Dysfunctions of the Iga system: a common link between intestinal and renal diseases.Cellular & molecular immunology · 2011Review
- Toll-like receptor 4 expression is increased in circulating mononuclear cells of patients with immunoglobulin A nephropathy.Clinical and experimental immunology · 2010Article
- Uteroglobin interacts with the heparin-binding site of fibronectin and prevents fibronectin-IgA complex formation found in IgA-nephropathy.FEBS letters · 2008Article
- Increased Goodpasture antigen-binding protein expression induces type IV collagen disorganization and deposit of immunoglobulin A in glomerular basement membrane.The American journal of pathology · 2007 · on this mapArticle
- Fcalpha receptor (CD89) mediates the development of immunoglobulin A (IgA) nephropathy (Berger's disease). Evidence for pathogenic soluble receptor-Iga complexes in patients and CD89 transgenic mice.The Journal of experimental medicine · 2000Article
- Imbalances in serum proinflammatory cytokines and their soluble receptors: a putative role in the progression of idiopathic IgA nephropathy (IgAN) and Henoch-Schönlein purpura nephritis, and a potential target of immunoglobulin therapy?Clinical and experimental immunology · 1998Article
- Antineutrophil cytoplasm antibodies (ANCA) of IgA isotype in adult Henoch-Schönlein purpura.Clinical and experimental immunology · 1994Article
- Nephrology, dialysis and transplantation.Postgraduate medical journal · 1993Review
- Pathogenesis of idiopathic IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 1993Review
- Autoimmunity and glomerulonephritis.Postgraduate medical journal · 1992Review
- Mesangial cell autoantigens in immunoglobulin A nephropathy and Henoch-Schönlein purpura.The Journal of clinical investigation · 1991Article
- Evidence that the interaction between circulating IgA and fibronectin is a normal process enhanced in primary IgA nephropathy.Journal of clinical immunology · 1991Article
- Fibronectin-immunoglobulin complexes in the early course of IgA and Henoch-Schönlein nephritis.Pediatric nephrology (Berlin, Germany) · 1991Article
- The structure and function of human IgA.The Biochemical journal · 1990Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgA antibodies from patients with primary IgA nephropathy bind to collagens I, II, and IV. Here we show that this binding is mediated by the collagen-binding site of fibronectin, which occurs in the circulation in complex with IgA. No antibodies binding directly to collagen were identified. The complexes were isolated by affinity chromatography on gelatin-Sepharose and heparin-Sepharose, both with affinity for fibronectin, followed by adsorption to anti-human IgA immobilized on agarose gel. The presence of fibronectin and IgA antibodies in the isolated complexes is shown by enzyme-linked immunosorbent assay, gel electrophoresis, and electrophoretic transfer followed by immunostaining. The presence of an IgA-fibronectin complex in serum and the binding of this complex to collagen demonstrate the necessity of removing fibronectin from serum prior to identifying anti-collagen antibodies.
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