ArticleLife science alliance2024
Oral bacteria induce IgA autoantibodies against a mesangial protein in IgA nephropathy model mice.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Principles for Optimal Drug Selection in IgA Nephropathy-Time for Integrating Pathogenesis and Clinical Markers to Guide Therapy.Nephrology (Carlton, Vic.) · 2026Review
- Serum anti-β2 spectrin IgA antibodies are produced in a CD4 T cell-independent manner in IgA nephropathy model mouse.Frontiers in immunology · 2026Article
- Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026Review
- Membranous nephropathy as a segmental pattern with solitary immunoglobulin A deposition: a case report.CEN case reports · 2025Article
- Review
- Glomerular Galactose-Deficient IgA1 Deposition in 192 Autopsy Cases in Japan.Nephrology (Carlton, Vic.) · 2025Article
- Carboxymethyl-lysine is a Prominent Target of Circulating IgA in IgA Nephropathy.Kidney international reports · 2025Article
- The Prevalence and Characteristics of IgA Antibodies to β2-Spectrin and CBX3 in Immunoglobulin A Nephropathy.Kidney international reports · 2025Article
- The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk.Theranostics · 2025Review
- Immune Cell Characteristics in a Gut-Kidney Axis-Induced Mouse Model of IgA Nephropathy: The Upregulated Dendritic Cells and Neutrophils.Journal of inflammation research · 2025Article
- Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024Review
- IgA Nephropathy: Significance of IgA1-Containing Immune Complexes in Clinical Settings.Journal of clinical medicine · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgA nephropathy (IgAN) is caused by deposition of IgA in the glomerular mesangium. The mechanism of selective deposition and production of IgA is unclear; however, we recently identified the involvement of IgA autoantibodies. Here, we show that CBX3 is another self-antigen for IgA in gddY mice, a spontaneous IgAN model, and in IgAN patients. A recombinant antibody derived from gddY mice bound to CBX3 expressed on the mesangial cell surface in vitro and to glomeruli in vivo. An elemental diet and antibiotic treatment decreased the levels of autoantibodies and IgAN symptoms in gddY mice. Serum IgA and the recombinant antibody from gddY mice also bound to oral bacteria of the mice and binding was competed with CBX3. One species of oral bacteria was markedly decreased in elemental diet-fed gddY mice and induced anti-CBX3 antibody in normal mice upon immunization. These data suggest that particular oral bacteria generate immune responses to produce IgA that cross-reacts with mesangial cells to initiate IgAN.
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