ReviewFrontiers in immunology2023
Current understanding of IgA antibodies in the pathogenesis of IgA nephropathy.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- Efficacy and safety of agents for IgA nephropathy: a network meta-analysis of randomized controlled trials.Frontiers in medicine · 2025Pooled it
- Risk factors and outcomes of IgA nephropathy recurrence after kidney transplantation: a systematic review and meta-analysis.Frontiers in immunology · 2023Pooled it
- Effect of DailyMedicina (Kaunas, Lithuania) · 2025Trial
- Clinical characteristics and prognosis of IgA nephropathy and comorbid diabetic kidney disease.Annals of medicine · 2026Article
- Mechanism-centered target discovery across glomerulonephritis phenotypes: an integrative multi-omics study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Structural promiscuity in the human circulatory IgA1 clonal repertoire.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Kidney Transcriptomic and Proteomic Analyses Provide New Insight into the Pathogenesis of IgA Nephropathy in Mice.Biochemical genetics · 2026Article
- Prolonged skin involvement distinguishes adolescent from childhood-onset IgA vasculitis: a large multicenter study with 687 patients.Advances in rheumatology (London, England) · 2026Article
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
- Mechanistic Insights and Therapeutic Advances of Anti-Inflammatory Biologics in Immune-Mediated Glomerulonephritis: A Narrative Review.Journal of inflammation research · 2026Review
- Spatially microdissected profiling of tonsillar germinal centers reveals a KLRG1-enriched immune signature in IgA nephropathy.Frontiers in immunology · 2026Article
- Transcriptome profiling indicates varied gene responses to Pasteurella multocida mutant infections in cattle.PloS one · 2026Article
- Histone methylation of kidney disease: fact or fantasy?Renal failure · 2025Review
- Investigating the genetic effects of metformin-related targets on IgA nephropathy using Mendelian randomization.Renal failure · 2025Article
- MYC affects mitochondrial function in IgA nephropathy by promoting the degradation of MFN1 through HRD1.Immunologic research · 2025Article
- Bilateral vision loss as first clinical manifestation of IgA nephropathy.BMC ophthalmology · 2025Article
- B Cell Activating Factor Does Not Play a Pivotal Role in the Synthesis of Aberrantly Glycosylated IgA.Nephrology (Carlton, Vic.) · 2025Article
- Comprehensive analysis of the clinical and pathological features and prognoses of children with immunoglobulin A vasculitis nephritis with immunoglobulin M deposits in glomeruli.Kidney research and clinical practice · 2025Article
- Review
- Serum Peroxiredoxins Reflect Oxidative Stress and Predict Renal Outcomes in Patients with Glomerulonephritis.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A (IgA) is the most abundant isotype of antibodies, provides a first line of defense at mucosal surfaces against pathogens, and thereby contributes to mucosal homeostasis. IgA is generally considered as a non-inflammatory antibody because of its main function, neutralizing pathogenic virus or bacteria. Meanwhile, IgA can induce IgA-mediated diseases, such as IgA nephropathy (IgAN) and IgA vasculitis. IgAN is characterized by the deposition of IgA and complement C3, often with IgG and/or IgM, in the glomerular mesangial region, followed by mesangial cell proliferation and excessive synthesis of extracellular matrix in glomeruli. Almost half a century has passed since the first report of patients with IgAN; it remains debatable about the mechanism how IgA antibodies selectively bind to mesangial region-a hallmark of IgAN-and cause glomerular injuries in IgAN. Previous lectin- and mass-spectrometry-based analysis have revealed that IgAN patients showed elevated serum level of undergalactosylated IgA1 in O-linked glycans of its hinge region, called galactose-deficient IgA1 (Gd-IgA1). Thereafter, numerous studies have confirmed that the glomerular IgA from IgAN patients are enriched with Gd-IgA1; thus, the first hit of the current pathogenesis of IgAN has been considered to increase circulating levels of Gd-IgA1. Recent studies, however, demonstrated that this aberrant glycosylation alone is not sufficient to disease onset and progression, suggesting that several additional factors are required for the selective deposition of IgA in the mesangial region and induce nephritis. Herein, we discuss the current understanding of the characteristics of pathogenic IgA and its mechanism of inducing inflammation in IgAN.
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