ArticleClinical and experimental immunology2001
T cell cytokines determine the severity of experimental IgA nephropathy by regulating IgA glycosylation.
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 63 citations in OpenAlex.
- Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.CEN case reports · 2026Article
- Detailed Pathophysiology of Minimal Change Disease: Insights into Podocyte Dysfunction, Immune Dysregulation, and Genetic Susceptibility.International journal of molecular sciences · 2024Review
- Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024Review
- Sequential administration of paricalcitol followed by IL-17 blockade for progressive refractory IgA nephropathy patients.Scientific reports · 2024Article
- History of IgA Nephropathy Mouse Models.Journal of clinical medicine · 2021Review
- Serum interferon-γ and urinary monocyte chemoattractant peptide-1 are important factors in the pathogenesis of immunoglobulin A nephropathy.Kidney research and clinical practice · 2021Article
- Primary IgA nephropathy: current challenges and future prospects.International journal of nephrology and renovascular disease · 2018Review
- Immunoglobulin A nephropathy: a pathophysiology view.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Review
- Effect of Immunosuppressive Drugs on the Changes of Serum Galactose-Deficient IgA1 in Patients with IgA Nephropathy.PloS one · 2016Observational
- Genetic Variation in miR-146a Is Not Associated with Susceptibility to IgA Nephropathy in Adults from a Chinese Han Population.PloS one · 2015Article
- Henoch-Schönlein purpura nephritis in children.Nature reviews. Nephrology · 2014Review
- Development of Animal Models of Human IgA Nephropathy.Drug discovery today. Disease models · 2014Article
- Antiviral innate immunity disturbs podocyte cell function.Journal of innate immunity · 2013Article
- Disruption of Smad4 expression in T cells leads to IgA nephropathy-like manifestations.PloS one · 2013Article
- Protective Effect of Stachybotrys microspora Triprenyl Phenol-7on the Deposition of IgA to the Glomerular Mesangium in Nivalenol-induced IgA Nephropathy Using BALB/c Mice.Journal of toxicologic pathology · 2012Article
- IgG3 deficiency extends lifespan and attenuates progression of glomerulonephritis in MRL/lpr mice.Biology direct · 2012Article
- Genetics and immunopathogenesis of IgA nephropathy.Clinical reviews in allergy & immunology · 2011Review
- Down-regulation of core 1 beta1,3-galactosyltransferase and Cosmc by Th2 cytokine alters O-glycosylation of IgA1.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2010Article
- Tissue deposits of IgA-binding streptococcal M proteins in IgA nephropathy and Henoch-Schonlein purpura.The American journal of pathology · 2010Article
- T cell cytokine polarity as a determinant of immunoglobulin A (IgA) glycosylation and the severity of experimental IgA nephropathy.Clinical and experimental immunology · 2008Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Hyperfunction of Th2 cells and aberrant glycosylation of IgA have been proposed independently as factors in the pathogenesis of IgA nephropathy (IgAN), the most common form of glomerulonephritis. To investigate the relationship between Th2 cytokines and IgA glycosylation in the genesis of IgAN, we induced IgAN in C3HeB and BALB/c mice by oral immunization and intranasal challenge with Sendai virus. Although both strains of mice developed microhaematuria and glomerular IgA immune deposits to similar degrees, only BALB/c mice developed significant renal insufficiency. More profound reductions of terminal galactosylation and sialylation occurred in Sendai virus-specific IgA from BALB/c versus C3HeB mice, and splenocytes from immunized BALB/c mice produced more Th2 and less Th1 cytokines compared to C3HeB mice when stimulated with antigen in vitro. Furthermore, the decreased glycosylation of IgA elicited by Th2 cytokines in vitro was blunted by the addition of IFN-gamma. We conclude that increased production of Th2 cytokines can lead to abnormalities in IgA glycosylation, which in turn promote heightened phlogistic responses to IgA immune complexes lodging in the glomerulus. We suggest that a relative or absolute increase in Th2 cytokine production in response to mucosal infection is a significant pathogenic factor in human IgAN.
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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.