ArticlePloS one2014
Uncoupling of glomerular IgA deposition and disease progression in alymphoplasia mice with IgA nephropathy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 8 citations in OpenAlex.
- Tissue-resident macrophages and renal diseases: landscapes and treatment directions.Frontiers in immunology · 2025Review
- Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024Review
- IgA nephropathy associated with Crohn's disease.World journal of methodology · 2023Review
- Mucosal Immune System Dysregulation in the Pathogenesis of IgA Nephropathy.Biomedicines · 2022Review
- Are there animal models of IgA nephropathy?Seminars in immunopathology · 2021Review
- Clinical effects of perazine ferulate tablets combined with eucalyptol limonene pinene enteric soft capsules for treatment of children with IgA nephropathy.Experimental and therapeutic medicine · 2016Article
- Pathogenic Role of a Proliferation-Inducing Ligand (APRIL) in Murine IgA Nephropathy.PloS one · 2015Article
- The kinetics of glomerular deposition of nephritogenic IgA.PloS one · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous clinical and experimental studies have indicated that cells responsible for IgA nephropathy (IgAN), at least in part, are localized in bone marrow (BM). Indeed, we have demonstrated that murine IgAN can be experimentally reconstituted by bone marrow transplantation (BMT) from IgAN prone mice in not only normal mice, but also in alymphoplasia mice (aly/aly) independent of IgA+ cells homing to mucosa or secondary lymphoid tissues. The objective of the present study was to further assess whether secondary lymph nodes (LN) contribute to the progression of this disease. BM cells from the several lines of IgAN prone mice were transplanted into aly/aly and wild-type mice (B6). Although the transplanted aly/aly showed the same degree of mesangial IgA and IgG deposition and the same serum elevation levels of IgA and IgA-IgG immune-complexes (IC) as B6, even in extent, the progression of glomerular injury was observed only in B6. This uncoupling in aly/aly was associated with a lack of CD4+ T cells and macrophage infiltration, although phlogogenic capacity to nephritogenic IC of renal resident cells was identical between both recipients. It is suggested that secondary LN may be required for the full progression of IgAN after nephritogenic IgA and IgA/IgG IC deposition.
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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.