ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Murine membranous nephropathy: immunization with α3(IV) collagen fragment induces subepithelial immune complexes and FcγR-independent nephrotic syndrome.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Animal models of idiopathic membranous nephropathy: Recent advances and future perspectives.Animal models and experimental medicine · 2026Review
- Successful Treatment of a 42-Year-Old Man with Concurrent Anti-Glomerular Basement Membrane Disease and Anti-Phospholipase A2 Receptor Antibody-Positive Membranous Nephropathy: A Case Report.The American journal of case reports · 2025Article
- Clinicopathological features and predictors of anti-GBM disease combined with membranous nephropathy.Clinical kidney journal · 2025Article
- Depletion of myeloid-derived suppressor cells alleviates kidney damage in murine membranous nephropathy.Frontiers in immunology · 2025Article
- Animal models of membranous nephropathy: more choices and higher similarity.Frontiers in immunology · 2024Review
- Epitope Spreading: The Underlying Mechanism for Combined Membranous Lupus Nephritis and Anti-GBM Disease?Case reports in nephrology · 2023Article
- Clinical and pathological features of anti-glomerular basement membrane disease associated with membranous nephropathy: an observational study.Renal failure · 2022Observational
- Case Report: Coexistence of Anti-Glomerular Basement Membrane Disease, Membranous Nephropathy, and IgA Nephropathy in a Female PatientWith Preserved Renal Function.Frontiers in pharmacology · 2022Article
- Membranous nephropathy: Clearer pathology and mechanisms identify potential strategies for treatment.Frontiers in immunology · 2022Review
- The Alternative Pathway Is Necessary and Sufficient for Complement Activation by Anti-THSD7A Autoantibodies, Which Are Predominantly IgG4 in Membranous Nephropathy.Frontiers in immunology · 2022Article
- How Times Have Changed! A Cornucopia of Antigens for Membranous Nephropathy.Frontiers in immunology · 2021Review
- Advances of the experimental models of idiopathic membranous nephropathy (Review).Molecular medicine reports · 2020Review
- Alternative Pathway Is Essential for Glomerular Complement Activation and Proteinuria in a Mouse Model of Membranous Nephropathy.Frontiers in immunology · 2018Article
- Basement membranes and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Optimizing the translational value of animal models of glomerulonephritis: insights from recent murine prototypes.American journal of physiology. Renal physiology · 2016Review
- Alternative Pathway Dysregulation and the Conundrum of Complement Activation by IgG4 Immune Complexes in Membranous Nephropathy.Frontiers in immunology · 2016Review
- Neonatal Fc receptor promotes immune complex-mediated glomerular disease.Journal of the American Society of Nephrology : JASN · 2014Article
- Quaternary epitopes of α345(IV) collagen initiate Alport post-transplant anti-GBM nephritis.Journal of the American Society of Nephrology : JASN · 2013Article
- Proteolysis breaks tolerance toward intact α345(IV) collagen, eliciting novel anti-glomerular basement membrane autoantibodies specific for α345NC1 hexamers.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Mouse models of membranous nephropathy: the road less travelled by.American journal of clinical and experimental immunology · 2013Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
Abstract
Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults and a significant cause of end-stage renal disease, yet current therapies are nonspecific, toxic, and often ineffective. The development of novel targeted therapies requires a detailed understanding of the pathogenic mechanisms, but progress is hampered by the lack of a robust mouse model of disease. We report that DBA/1 mice as well as congenic FcγRIII(-/-) and FcRγ(-/-) mice immunized with a fragment of α3(IV) collagen developed massive albuminuria and nephrotic syndrome, because of subepithelial deposits of mouse IgG and C3 with corresponding basement membrane reaction and podocyte foot process effacement. The clinical presentation and histopathologic findings were characteristic of MN. Although immunized mice produced genuine anti-α3NC1 autoantibodies that bound to kidney and lung basement membranes, neither crescentic glomerulonephritis nor alveolitis ensued, likely because of the predominance of mouse IgG1 over IgG2a and IgG2b autoantibodies. The ablation of activating IgG Fc receptors did not ameliorate injury, implicating subepithelial deposition of immune complexes and consequent complement activation as a major effector pathway. We have thus established an active model of murine MN. This model, leveraged by the availability of genetically engineered mice and mouse-specific reagents, will be instrumental in studying the pathogenesis of MN and evaluating the efficacy of novel experimental therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.