ArticlePloS one2015
Pathogenic Role of a Proliferation-Inducing Ligand (APRIL) in Murine IgA Nephropathy.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- A Phase 2 Trial of Sibeprenlimab in Patients with IgA Nephropathy.The New England journal of medicine · 2024Trial
- 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 new therapies: from data in adults to application in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Recent Advancements in the Therapeutic Landscape of IgA Nephropathy and the Impact of Dual Blockers: Telitacicept.Kidney medicine · 2026Review
- Review
- Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026Review
- B Cell Activating Factor Does Not Play a Pivotal Role in the Synthesis of Aberrantly Glycosylated IgA.Nephrology (Carlton, Vic.) · 2025Article
- Modern Biomarkers in IgA Nephropathy and Their Potential in Paediatric Research.Journal of clinical medicine · 2025Review
- Inhibitory effect of exercise on elevated blood pressure and fetal growth restriction during pregnancy in Dahl salt-sensitive rats.Physiological reports · 2025Article
- Patients With Immunoglobulin A Nephropathy Show Abnormal Frequencies of B Cell Subsets, Unconventional T Cells, and High Levels of Galactose-Deficient IgA1-Coated Gut Bacteria.Kidney international reports · 2025Article
- What is new in the pathogenesis and treatment of IgA glomerulonephritis.World journal of nephrology · 2024Review
- Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024Review
- Pathogenic Immunoglobulin A-Producing Cells in Immunoglobulin A Nephropathy.Journal of clinical medicine · 2024Review
- Intestinal epithelium dysfunctions cause IgA deposition in the kidney glomeruli of intestine-specific Ap1m2-deficient mice.EBioMedicine · 2024Article
- Unique and redundant roles of mouse BCMA, TACI, BAFF, APRIL, and IL-6 in supporting antibody-producing cells in different tissues.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Successful pregnancy in a patient with IgA nephropathy treated with telitacicept: a case report.BMC pregnancy and childbirth · 2024Article
- Contemporary review of IgA nephropathy.Frontiers in immunology · 2024Review
- The contribution of a proliferation-inducing ligand (APRIL) and other TNF superfamily members in pathogenesis and progression of IgA nephropathy.Clinical kidney journal · 2023Review
- A PRoliferation-Inducing Ligand (APRIL) in the Pathogenesis of Immunoglobulin A Nephropathy: A Review of the Evidence.Journal of clinical medicine · 2023Review
- The role of BAFF and APRIL in IgA nephropathy: pathogenic mechanisms and targeted therapies.Frontiers in nephrology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A proliferation-inducing ligand (APRIL) is a member of the tumor necrosis factor (TNF) superfamily. Despite advances in clinical and genetic studies, the details of the pathological roles of APRIL in IgA nephropathy (IgAN) remain to be fully defined. The present study aimed to further assess the pathological role of APRIL using a mouse model of IgAN. Mice with IgAN designated "grouped ddY" (gddY) were intraperitoneally administered an anti-APRIL monoclonal antibody (anti-APRIL Ab) or control IgG (Control Ab) twice each week for 2 weeks starting during the early stage of IgAN (6-7 weeks of age). Urinary albumin, serum IgA, and glomerular IgA deposition were evaluated. We further assessed the inflammatory responses during treatment by measuring the levels of the chemokine fractalkine (FKN) and its receptor CX3CR1 as well as the level of peripheral blood monocytosis. Anti-APRIL Ab treatment significantly decreased albuminuria and tissue damage combined with decreases in serum IgA levels and deposition of glomerular IgA. In contrast, the abundance of IgA+/B220+ or CD138+/B220+ B cells in the spleen and bone marrow, respectively, was unchanged. Treating gddY mice with anti-April Ab reduced the overexpression of FKN/CX3CR1 in the kidney and the increase in the population of circulating Gr1-/CD115+ monocytes. The size of the population of Gr1-/CD115+ monocytes correlated with renal FKN and urinary albumin levels. Moreover, mice treated with anti-APRIL Ab exhibited reduced progression of IgAN, serum IgA levels, and glomerular IgA deposition as well as an attenuated inflammatory process mediated by FKN-associated activation of monocytes. To the best of our knowledge, this is the first study to implicate the APRIL signal transduction pathway in the pathogenesis of nephrogenic IgA production. Moreover, our findings identify APRIL as a potential target of therapy.
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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.