ArticleNephrology (Carlton, Vic.)2025
B Cell Activating Factor Does Not Play a Pivotal Role in the Synthesis of Aberrantly Glycosylated IgA.
Article in Nephrology (Carlton, Vic.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- Targeting the B-Cell Activating Factor and a Proliferation-Inducing Ligand Pathway in IgAN: From Disease Pathogenesis to Clinical Trial Evidence.Kidney international reports · 2026Review
- IgA Nephropathy: Epidemiology, Outcomes, and Insights for Primary Glomerulonephritides.Journal of clinical medicine · 2026Review
- B Cell Activating Factor Does Not Play a Pivotal Role in the Synthesis of Aberrantly Glycosylated IgA.Nephrology (Carlton, Vic.) · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
aimIgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, yet its pathogenesis remains incompletely understood. B cell activating factor (BAFF), a TNF family member involved in B cell activation and IgA class switching, has been proposed as a potential pathogenic factor in IgAN. However, its role in disease progression is unclear. This study aimed to investigate the pathological role of BAFF in IgAN using grouped ddY (gddY) mice, a spontaneous murine model of IgAN.
methodsgddY mice were treated with anti-BAFF monoclonal antibody (anti-BAFF Ab) or PBS via intraperitoneal injection twice a week for 4 weeks. Urinary albumin, serum immunoglobulins, and IgA-IgG immune complex were measured pre- and post-treatment. Serum levels of aberrantly glycosylated IgA were quantified using specific lectin-based assays. Glomerular IgA and C3 depositions were evaluated by immunofluorescence, and B cell populations in spleen and bone marrow were analysed by flowcytometry.
resultsAnti-BAFF Ab treatment significantly reduced serum IgA, IgG, and IgM levels as compared with PBS treatment (p < 0.001, p = 0.003, and p = 0.002, respectively). However, it did not affect serum aberrantly glycosylated IgA, IgA-IgG immune complex, and urinary albumin excretion. Glomerular depositions of IgA and C3 as well as B cell population in the spleen and bone marrow were also not affected by anti-BAFF Ab treatment.
conclusionBAFF inhibition reduces general immunoglobulin levels but does not impact nephritogenic IgA production or disease progression in murine IgAN. These findings suggest that BAFF-dependent IgA production may not be involved in the pathogenesis of IgAN.
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Registered trials
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