ArticlePloS one2013
Disruption of Smad4 expression in T cells leads to IgA nephropathy-like manifestations.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Serum soluble interleukin-2 receptor alpha may predict tubulointerstitial inflammatory cell infiltration and short-term disease progression in immunoglobin A nephropathy.Immunologic research · 2024Article
- Intestinal epithelium dysfunctions cause IgA deposition in the kidney glomeruli of intestine-specific Ap1m2-deficient mice.EBioMedicine · 2024Article
- Sequential administration of paricalcitol followed by IL-17 blockade for progressive refractory IgA nephropathy patients.Scientific reports · 2024Article
- Review
- Consequences of Mutations and Abnormal Expression of SMAD4 in Tumors and T Cells.OncoTargets and therapy · 2021Review
- T lymphocytes in IgA nephropathy.Experimental and therapeutic medicine · 2020Article
- Paraneoplastic immunoglobulin A nephropathy and associated focal segmental glomerulosclerosis in asymptomatic low volume B-cell lymphoma - a case report.BMC nephrology · 2018Article
- Inhibition of STAT3 Signaling Reduces IgA1 Autoantigen Production in IgA Nephropathy.Kidney international reports · 2017Article
- Henoch-Schönlein purpura nephritis in children.Nature reviews. Nephrology · 2014Review
- Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The link between glomerular IgA nephropathy (IgAN) and T helper 2 (Th2) response has been implicated, however, the mechanisms are poorly defined because of the lack of an appropriate model. Here we report a novel murine model characterized by lineage-restricted deletion of the gene encoding MAD homologue 4 (Smad4) in T cells (Smad4(co/co;Lck-cre) ). Loss of Smad4 expression in T cells results in overproduction of Th2 cytokines and high serum IgA levels. We found that Smad4(co/co;Lck-cre) mice exhibited massive glomerular IgA deposition, increased albumin creatinine ratio, aberrant glycosylated IgA, IgA complexed with IgG1 and IgG2a, and polymeric IgA, all known features of IgAN in humans. Furthermore, we examined the β1, 4-galactosyltransferases (β4GalT) enzyme which is involved in the synthesis of glycosylated murine IgA, and we found reduced β4GalT2 and β4GalT4 mRNA levels in B cells. These findings indicate that Smad4(co/co;Lck-cre) mice could be a useful model for studying the mechanisms between IgAN and Th2 response, and further, disruption of Smad4-dependent signaling in T cells may play an important role in the pathogenesis of human IgAN and contributing to a Th2 T cell phenotype.
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Registered trials
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