ArticleJCI insight2017
B cell-derived IL-4 acts on podocytes to induce proteinuria and foot process effacement.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.
- Meta-analysis of the efficacy of rituximab in the management of cryoglobulinemic vasculitis.Frontiers in medicine · 2025Pooled it
- The Efficacy and Safety of Rituximab for Childhood Steroid-Dependent Nephrotic Syndrome: A Systematic Review and Meta-Analysis.Frontiers in pediatrics · 2021Pooled it
- The role of interleukin-4 in acute kidney injury and chronic kidney disease: a literature review.BMC nephrology · 2026Review
- Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026Review
- Immune podocyte injury in autoimmune glomerular diseases.Frontiers in immunology · 2026Review
- TGF-β in chronic kidney disease: a controversy for decades.Frontiers in immunology · 2026Review
- The Use of Rituximab in Glomerulonephritis: What Is the Evidence?Biomedicines · 2025Review
- Article
- Protective Effects ofBiomedicines · 2025Article
- Rituximab as a first-line therapy in children with new-onset idiopathic nephrotic syndrome.Clinical kidney journal · 2025Article
- Impact of atopic dermatitis on renal dysfunction: insights from patient data and animal models.Frontiers in immunology · 2025Article
- Forging the Future: B Cell Activating Factor's Impact on Nephrotic Syndrome.The Malaysian journal of medical sciences : MJMS · 2024Review
- The Pathogenesis of Nephrotic Syndrome: A Perspective from B Cells.Kidney diseases (Basel, Switzerland) · 2024Review
- Longitudinal intravital microscopy of the mouse kidney: inflammatory responses to abdominal imaging windows.American journal of physiology. Renal physiology · 2024Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes.Cells · 2024Review
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- The ion transporter NaScience advances · 2023Article
- Sexual dimorphism in acute myocardial infarction-induced acute kidney injury: cardiorenal deteriorating effects of ovariectomy in premenopausal female mice.Clinical science (London, England : 1979) · 2023Article
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
The efficacy of B cell depletion therapies in diseases such as nephrotic syndrome and rheumatoid arthritis suggests a broader role in B cells in human disease than previously recognized. In some of these diseases, such as the minimal change disease subtype of nephrotic syndrome, pathogenic antibodies and immune complexes are not involved. We hypothesized that B cells, activated in the kidney, might produce cytokines capable of directly inducing cell injury and proteinuria. To directly test our hypothesis, we targeted a model antigen to the kidney glomerulus and showed that transfer of antigen-specific B cells could induce glomerular injury and proteinuria. This effect was mediated by IL-4, as transfer of IL-4-deficient B cells did not induce proteinuria. Overexpression of IL-4 in mice was sufficient to induce kidney injury and proteinuria and could be attenuated by JAK kinase inhibitors. Since IL-4 is a specific activator of STAT6, we analyzed kidney biopsies and demonstrated STAT6 activation in up to 1 of 3 of minimal change disease patients, suggesting IL-4 or IL-13 exposure in these patients. These data suggest that the role of B cells in nephrotic syndrome could be mediated by cytokines.
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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.