ArticleThe Journal of biological chemistry2014
Cytokines alter IgA1 O-glycosylation by dysregulating C1GalT1 and ST6GalNAc-II enzymes.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 2 of them syntheses that pooled it.
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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
115 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.
- Ascertaining the mechanistic etiology of COVID-associated glomerulonephritis: a systematic review.Frontiers in medicine · 2025Pooled it
- Association of Immune and Inflammatory Gene Polymorphism With the Risk of IgA Nephropathy: A Systematic Review and Meta-Analysis of 45 Studies.Frontiers in immunology · 2021Pooled it
- Galactose-deficient IgA1 and the corresponding IgG autoantibodies predict IgA nephropathy progression.PloS one · 2019Trial
- A Randomized, Controlled Trial of Rituximab in IgA Nephropathy with Proteinuria and Renal Dysfunction.Journal of the American Society of Nephrology : JASN · 2017Trial
- Microplastics and IgA nephropathy: a novel environmental hypothesis of immune dysregulation.Renal failure · 2026Review
- Kidney pathology findings in pediatric patients with kidney injury and inflammatory bowel disease: a case series.Pediatric nephrology (Berlin, Germany) · 2026Article
- Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.CEN case reports · 2026Article
- Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression ofbioRxiv : the preprint server for biology · 2026Article
- A case of IgA vasculitis developing in a patient with Crohn's disease treated with adalimumab.Clinical journal of gastroenterology · 2026Article
- Article
- Modified Huangqi Chifeng decoction alleviates IgA nephropathy inflammation and renal fibrosis via miR-146a/TLR4/NF-κB signaling modulation.Frontiers in immunology · 2026Article
- New Insights on IgA Nephropathy from the Perspective of Active Lesions and Systemic Inflammatory Responses.ImmunoTargets and therapy · 2026Review
- Aberrant signaling in tonsillar B cells producing pathogenicFrontiers in immunology · 2026Review
- Gut-kidney axis in IgA nephropathy: mechanisms linking microbiota dysbiosis to immune dysregulation, Gd-IgA1 generation, and renal injury.Frontiers in immunology · 2026Review
- TLR7/9-mediated mucosal innate immune dysregulation in IgA nephropathy.Frontiers in immunology · 2026Review
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
- Dioscin attenuates Gd-IgA1 overproduction by inhibiting the IL-6-JAK2/STAT3 signaling axis in IgA nephropathy.BMC nephrology · 2025Article
- Transcriptomic Patterns in Adult and Pediatric Patients with IgA Nephropathy or IgA Vasculitis with Nephropathy.Journal of the American Society of Nephrology : JASN · 2025Article
- SOCS1 improves abnormal IgA galactosylation in IgA nephropathy by regulating the TLR9/MyD88 pathway.Immunologic research · 2025Article
- Longitudinal changes in the abundance of IgA1 O- and N-glycoforms in IgA nephropathy.Clinical and experimental nephrology · 2025Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
IgA nephropathy (IgAN), the most common primary glomerulonephritis, is characterized by renal immunodeposits containing IgA1 with galactose-deficient O-glycans (Gd-IgA1). These immunodeposits originate from circulating immune complexes consisting of anti-glycan antibodies bound to Gd-IgA1. As clinical disease onset and activity of IgAN often coincide with mucosal infections and dysregulation of cytokines, we hypothesized that cytokines may affect IgA1 O-glycosylation. We used IgA1-secreting cells derived from the circulation of IgAN patients and healthy controls and assessed whether IgA1 O-glycosylation is altered by cytokines. Of the eight cytokines tested, only IL-6 and, to a lesser degree, IL-4 significantly increased galactose deficiency of IgA1; changes in IgA1 O-glycosylation were robust for the cells from IgAN patients. These cytokines reduced galactosylation of the O-glycan substrate directly via decreased expression of the galactosyltransferase C1GalT1 and, indirectly, via increased expression of the sialyltransferase ST6GalNAc-II, which prevents galactosylation by C1GalT1. These findings were confirmed by siRNA knockdown of the corresponding genes and by in vitro enzyme reactions. In summary, IL-6 and IL-4 accentuated galactose deficiency of IgA1 via coordinated modulation of key glycosyltransferases. These data provide a mechanism explaining increased immune-complex formation and disease exacerbation during mucosal infections in IgAN patients.
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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.