ArticleJournal of the American Society of Nephrology : JASN2014
Neonatal Fc receptor promotes immune complex-mediated glomerular disease.
Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Blocking FcRn in humans reduces circulating IgG levels and inhibits IgG immune complex-mediated immune responses.Science advances · 2019Trial
- M281, an Anti-FcRn Antibody: Pharmacodynamics, Pharmacokinetics, and Safety Across the Full Range of IgG Reduction in a First-in-Human Study.Clinical pharmacology and therapeutics · 2019Trial
- Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Endosome traffic in rheumatic diseases: mechanistic insights and therapeutic opportunities.Nature reviews. Rheumatology · 2026Review
- The FcRn from gene to protein and function: comparison between species.Frontiers in immunology · 2025Review
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- Exploiting the neonatal crystallizable fragment receptor to treat kidney disease.Kidney international · 2024Review
- The fate of immune complexes in membranous nephropathy.Frontiers in immunology · 2024Review
- The therapeutic age of the neonatal Fc receptor.Nature reviews. Immunology · 2023Review
- Anti-phospholipase A2 receptor antibodies directly induced podocyte damageRenal failure · 2022Article
- The Collagen Receptor Discoidin Domain Receptor 1b Enhances Integrin β1-Mediated Cell Migration by Interacting With Talin and Promoting Rac1 Activation.Frontiers in cell and developmental biology · 2022Article
- In Translation: FcRn across the Therapeutic Spectrum.International journal of molecular sciences · 2021Review
- "Ways in which the neonatal Fc-receptor is involved in autoimmunity".Journal of translational autoimmunity · 2021Review
- Article
- Maternal alloimmune IgG causes anti-glomerular basement membrane disease in perinatal transgenic mice that express human laminin α5.Kidney international · 2019Article
- Knockout of the neonatal Fc receptor in cultured podocytes alters IL-6 signaling and the actin cytoskeleton.American journal of physiology. Cell physiology · 2019Article
- The Neonatal Fc Receptor (FcRn): A Misnomer?Frontiers in immunology · 2019Review
- In vivo depletion of serum IgG by an affibody molecule binding the neonatal Fc receptor.Scientific reports · 2018Article
- Alternative Pathway Is Essential for Glomerular Complement Activation and Proteinuria in a Mouse Model of Membranous Nephropathy.Frontiers in immunology · 2018Article
- Membranous glomerulonephropathy in a patient with bullous pemphigoid.CEN case reports · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
The neonatal Fc receptor (FcRn) is a major regulator of IgG and albumin homeostasis systemically and in the kidneys. We investigated the role of FcRn in the development of immune complex-mediated glomerular disease in mice. C57Bl/6 mice immunized with the noncollagenous domain of the α3 chain of type IV collagen (α3NC1) developed albuminuria associated with granular capillary loop deposition of exogenous antigen, mouse IgG, C3 and C5b-9, and podocyte injury. High-resolution imaging showed abundant IgG deposition in the expanded glomerular basement membrane, especially in regions corresponding to subepithelial electron dense deposits. FcRn-null and -humanized mice immunized with α3NC1 developed no albuminuria and had lower levels of serum IgG anti-α3NC1 antibodies and reduced glomerular deposition of IgG, antigen, and complement. Our results show that FcRn promotes the formation of subepithelial immune complexes and subsequent glomerular pathology leading to proteinuria, potentially by maintaining higher serum levels of pathogenic IgG antibodies. Therefore, reducing pathogenic IgG levels by pharmacologic inhibition of FcRn may provide a novel approach for the treatment of immune complex-mediated glomerular diseases. As proof of concept, we showed that a peptide inhibiting the interaction between human FcRn and human IgG accelerated the degradation of human IgG anti-α3NC1 autoantibodies injected into FCRN-humanized mice as effectively as genetic ablation of FcRn, thus preventing the glomerular deposition of immune complexes containing human IgG.
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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.