ArticleBMC nephrology2017
Pathogenic role of glycan-specific IgG antibodies in IgA nephropathy.
Article in BMC nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Lysosome-mediated aggregation of galactose-deficient IgA1 with transferrin receptor 1 links to IgA nephropathy.Nature communications · 2025Article
- What is new in the pathogenesis and treatment of IgA glomerulonephritis.World journal of nephrology · 2024Review
- Current understanding of IgA antibodies in the pathogenesis of IgA nephropathy.Frontiers in immunology · 2023Review
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- Intrarenal Single-Cell Sequencing of Hepatitis B Virus Associated Membranous Nephropathy.Frontiers in medicine · 2022Article
- A Partial Picture of the Single-Cell Transcriptomics of Human IgA Nephropathy.Frontiers in immunology · 2021Article
- Perspectives on how mucosal immune responses, infections and gut microbiome shape IgA nephropathy and future therapies.Theranostics · 2020Review
- Clinical significance of mesangial IgM deposition in patients with IgA nephropathy.Clinical and experimental nephrology · 2019Article
- Recurrent andFrontiers in immunology · 2019Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulating evidences proved the important roles of circulating IgA1-containing immune complexes (cIgA1) in IgA nephropathy (IgAN). Galactose-deficient IgA1 (Gd-IgA1) and glycan-specific IgG antibody have been identified as major components in cIgA1. Before, Gd-IgA1 was reported as a vital factor in IgAN, partly via of its pathogenic role to induce mesangial cells activation. However, we still lack direct evidences to clarify the biological effect of glycan-specific IgG antibody in IgAN.
methodsIn the present study, we enrolled 35 IgAN patients and 17 age- and sex-matched healthy controls. Using uniform aberrant glycosylated IgA1 molecules, and IgG from different individuals, we in vitro prepared IgG-ddIgA1 complexes, and compared the biological differences among these immune complexes regarding their proliferative and inflammatory effects on mesangial cells.
resultsIgG-ddIgA1 complexes from both patients with IgA nephropathy (IgAN-IgG-dd-IgA1) and healthy controls (HC-IgG-dd-IgA1) could induce the proliferation of mesangial cells and up-regulate expression of MCP-1, IL-6 and CXCL1. The levels of mesangial cells proliferation induced by IgAN-IgG-dd-IgA1 were significantly higher than those induced by HC-IgG-dd-IgA1 (1.10 ± 0.05 vs. 1.03 ± 0.03; p < 0.001). However, the levels of secreted MCP-1, IL-6 and CXCL1 from mesangial cells challenged by IgAN-IgG-dd-IgA1 and HC-IgG-dd-IgA1 were comparable.
conclusionsWe found that glycan-specific IgG antibodies derived from patients with IgAN had the biological effect to induce mesangial cells proliferation. Moreover, in the present study we also established a method for in vitro preparation of pathogenic IgG-ddIgA1 complexes, which could be applied in future studies exploring IgAN pathogenesis.
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