ArticleThe Journal of experimental medicine2012
Transglutaminase is essential for IgA nephropathy development acting through IgA receptors.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.
- Finerenone in IgA nephropathy: a systematic review and meta-analysis.BMC nephrology · 2026Pooled it
- Combined C4d and CD3 immunostaining predicts immunoglobulin (Ig)A nephropathy progression.Clinical and experimental immunology · 2015Trial
- 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
- Precision targeting of gut-kidney axis: mucosal immunomodulation in IgA nephropathy-a perspective.Frontiers in medicine · 2026Article
- TLR7/9-mediated mucosal innate immune dysregulation in IgA nephropathy.Frontiers in immunology · 2026Review
- Gd-IgA1-targeting therapy in IgA nephropathy ~what is pathogenic Gd-IgA1?~.Frontiers in nephrology · 2026Review
- Evaluation of Endocan, endothelial nitric oxide synthase, and solubleCD89 in children with IgA vasculitis.Clinical rheumatology · 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
- The pathogenesis of IgA nephropathy and implications for treatment.Nature reviews. Nephrology · 2025Review
- Blockade of mTOR ameliorates IgA nephropathy by correcting CD89 and CD71 dysfunctions in humanized mice.PloS one · 2025Article
- Characteristics, pathogenic and therapeutic role of gut microbiota in immunoglobulin A nephropathy.Frontiers in immunology · 2025Review
- 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
- Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024Review
- Experimental models for preclinical research in kidney disease.Zoological research · 2024Review
- Navigating Adult-Onset IgA Vasculitis-Associated Nephritis.Life (Basel, Switzerland) · 2024Review
- Heterozygous mutations in factor H aggravate pathological damage in a stable IgA deposition model induced byFrontiers in immunology · 2024Article
- Molecular Differences in Glomerular Compartment to Distinguish Immunoglobulin A Nephropathy and Lupus Nephritis.Journal of inflammation research · 2024Article
- Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgA nephropathy (IgAN) is a common cause of renal failure worldwide. Treatment is limited because of a complex pathogenesis, including unknown factors favoring IgA1 deposition in the glomerular mesangium. IgA receptor abnormalities are implicated, including circulating IgA-soluble CD89 (sCD89) complexes and overexpression of the mesangial IgA1 receptor, TfR1 (transferrin receptor 1). Herein, we show that although mice expressing both human IgA1 and CD89 displayed circulating and mesangial deposits of IgA1-sCD89 complexes resulting in kidney inflammation, hematuria, and proteinuria, mice expressing IgA1 only displayed endocapillary IgA1 deposition but neither mesangial injury nor kidney dysfunction. sCD89 injection into IgA1-expressing mouse recipients induced mesangial IgA1 deposits. sCD89 was also detected in patient and mouse mesangium. IgA1 deposition involved a direct binding of sCD89 to mesangial TfR1 resulting in TfR1 up-regulation. sCD89-TfR1 interaction induced mesangial surface expression of TGase2 (transglutaminase 2), which in turn up-regulated TfR1 expression. In the absence of TGase2, IgA1-sCD89 deposits were dramatically impaired. These data reveal a cooperation between IgA1, sCD89, TfR1, and TGase2 on mesangial cells needed for disease development. They demonstrate that TGase2 is responsible for a pathogenic amplification loop facilitating IgA1-sCD89 deposition and mesangial cell activation, thus identifying TGase2 as a target for therapeutic intervention in this disease.
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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.