ArticleJournal of the American Society of Nephrology : JASN2012
O-glycosylated IgA rheumatoid factor induces IgA deposits and glomerulonephritis.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Development and Evaluation of a Robust Sandwich Immunoassay System Detecting Serum WFA-Reactive IgA1 for Diagnosis of IgA Nephropathy.International journal of molecular sciences · 2022Article
- Quantitative analysis of protein crotonylation identifies its association with immunoglobulin A nephropathy.Molecular medicine reports · 2020Article
- IgA Structure Variations Associate with Immune Stimulations and IgA Mesangial Deposition.Journal of the American Society of Nephrology : JASN · 2016Article
- Optimizing the translational value of animal models of glomerulonephritis: insights from recent murine prototypes.American journal of physiology. Renal physiology · 2016Review
- Henoch-Schönlein purpura nephritis.Pediatric nephrology (Berlin, Germany) · 2015Review
- New insights into the pathogenesis of IgA nephropathy.Seminars in immunopathology · 2014Review
- O-linked glycosylation determines the nephritogenic potential of IgA rheumatoid factor.Journal of the American Society of Nephrology : JASN · 2014Article
- Article
- Development of Animal Models of Human IgA Nephropathy.Drug discovery today. Disease models · 2014Article
- Determination of severity of murine IgA nephropathy by glomerular complement activation by aberrantly glycosylated IgA and immune complexes.The American journal of pathology · 2012Article
- Development of a model of early-onset IgA nephropathy.Journal of the American Society of Nephrology : JASN · 2012Article
- Induction of IgA deposits and glomerulonephritis by IgA rheumatoid factor.Journal of the American Society of Nephrology : JASN · 2012Article
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7 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Structural aberrations of O-linked glycans present in the IgA1 hinge region are associated with IgA nephropathy, but their contribution to its pathogenesis remains incompletely understood. In this study, mice implanted with hybridoma secreting 6-19 IgA anti-IgG2a rheumatoid factor, but not 46-42 IgA rheumatoid factor bearing the same IgA allotype, developed mesangial deposits consisting of IgA, IgG2a, and C3. Studies in immunoglobulin- and C3-deficient mice revealed that the development of these glomerular lesions required the formation of IgA-IgG2a immune complexes and subsequent activation of complement. The proportion of polymeric and monomeric forms, the IgG2a-binding affinity, and the serum levels of IgA-IgG2a immune complexes were similar between 6-19 IgA- and 46-42 IgA-injected mice. In contrast, the analysis of oligosaccharide structures revealed highly galactosylated O-linked glycans in the hinge region of 6-19 IgA and poorly O-glycosylated in the hinge region of 46-42 IgA. Furthermore, the structure of N-linked glycans in the CH1 domain was the complex type in 6-19 IgA and the hybrid type in 46-42 IgA. In summary, this study demonstrates the presence of O-linked glycans in the hinge region of mouse IgA and suggests that 6-19 IgA rheumatoid factor-induced GN could serve as an experimental model for IgA nephropathy.
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