ArticleThe Journal of experimental medicine2000
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.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 106 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
106 citing papers in PubMed, 247 citations in OpenAlex.
- IgA binding characteristics of golden hamster and ferret Fcα receptors.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- IgA nephropathy new therapies: from data in adults to application in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Atomistic scattering modeling of the solution structure of human dimeric IgA1 reveals a structural and mechanistic basis for IgA nephropathy.The Journal of biological chemistry · 2026Article
- IgA Nephropathy: Mechanisms, Risk Stratification, and Precision Therapy.Diagnostics (Basel, Switzerland) · 2026Review
- The role of mesenchymal stem cells in IgA nephropathy: current evidence and future directions.Stem cell research & therapy · 2026Review
- Gd-IgA1-targeting therapy in IgA nephropathy ~what is pathogenic Gd-IgA1?~.Frontiers in nephrology · 2026Review
- Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026Review
- Long non-coding RNA in IgA nephropathy: a comprehensive review.Renal failure · 2025Review
- Review
- Lysosome-mediated aggregation of galactose-deficient IgA1 with transferrin receptor 1 links to IgA nephropathy.Nature communications · 2025Article
- Recent advances in pathogenetic concepts and disease modeling of IgA nephropathy.Clinical kidney journal · 2025Review
- Enrichment of human IgA-coated bacterial vesicles in ulcerative colitis as a driver of inflammation.Nature communications · 2025Article
- IgA class-switched CD27-CD21+ B cells in IgA nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Biomarker understanding first lessons from drug development for IgA-driven autoimmune and fibrotic diseases.Cambridge prisms. Precision medicine · 2025Review
- Characteristics, pathogenic and therapeutic role of gut microbiota in immunoglobulin A nephropathy.Frontiers in immunology · 2025Review
- Blockade of mTOR ameliorates IgA nephropathy by correcting CD89 and CD71 dysfunctions in humanized mice.PloS one · 2025Article
- Integrative Network Pharmacology and Transcriptomics Reveal the Mechanism of Gui-Qi-Yi-Shen Granules in the Treatment of IgA Nephropathy.Drug design, development and therapy · 2025Article
- Lactobacillus casei Cell Wall Extract and Production of Galactose-Deficient IgA1 in a Humanized IGHA1 Mouse Model.Journal of the American Society of Nephrology : JASN · 2025Article
- The pathogenesis of IgA nephropathy and implications for treatment.Nature reviews. Nephrology · 2025Review
- Vascular injury derived apoptotic exosome-like vesicles trigger autoimmunity.Journal of translational autoimmunity · 2024Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of immunoglobulin A (IgA) nephropathy (IgAN), the most prevalent form of glomerulonephritis worldwide, involves circulating macromolecular IgA1 complexes. However, the molecular mechanism(s) of the disease remain poorly understood. We report here the presence of circulating soluble FcalphaR (CD89)-IgA complexes in patients with IgAN. Soluble CD89 was identified as a glycoprotein with a 24-kD backbone that corresponds to the expected size of CD89 extracellular domains. To demonstrate their pathogenic role, we generated transgenic (Tg) mice expressing human CD89 on macrophage/monocytes, as no CD89 homologue is found in mice. These mice spontaneously developed massive mesangial IgA deposition, glomerular and interstitial macrophage infiltration, mesangial matrix expansion, hematuria, and mild proteinuria. The molecular mechanism was shown to involve soluble CD89 released after interaction with IgA. This release was independent of CD89 association with the FcRgamma chain. The disease was induced in recombination activating gene (RAG)2(-/-) mice by injection of serum from Tg mice, and in severe combined immunodeficiency (SCID)-Tg mice by injection of patients' IgA. Depletion of soluble CD89 from serum abolished this effect. These results reveal the key role of soluble CD89 in the pathogenesis of IgAN and provide an in vivo model that will be useful for developing new treatments.
Indexed as
Identifiers
What OpenQuestion holds
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.