ArticlePloS one2016
Critical Role of Kupffer Cell CD89 Expression in Experimental IgA Nephropathy.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- IgA binding characteristics of golden hamster and ferret Fcα receptors.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Mesenchymal stem cells: a potential therapeutic strategy for IgA nephropathy.Frontiers in pharmacology · 2026Review
- Review
- Biomarker understanding first lessons from drug development for IgA-driven autoimmune and fibrotic diseases.Cambridge prisms. Precision medicine · 2025Review
- A genetically determined molecular switch modulates the anti-inflammatory potential of human IgA.Frontiers in immunology · 2025Article
- IgA-producing B cells in lung homeostasis and disease.Frontiers in immunology · 2023Review
- Targeting CD89 on tumor-associated macrophages overcomes resistance to immune checkpoint blockade.Journal for immunotherapy of cancer · 2022Article
- History of IgA Nephropathy Mouse Models.Journal of clinical medicine · 2021Review
- Pathogenesis of IgA Vasculitis: An Up-To-Date Review.Frontiers in immunology · 2021Review
- IgA and FcαRI: Versatile Players in Homeostasis, Infection, and Autoimmunity.ImmunoTargets and therapy · 2020Review
- Mesangial Deposition Can Strongly Involve Innate-Like IgA Molecules Lacking Affinity Maturation.Journal of the American Society of Nephrology : JASN · 2019Article
- IgA and FcαRI: Pathological Roles and Therapeutic Opportunities.Frontiers in immunology · 2019Review
- IgA nephropathy: clearance kinetics of IgA-containing immune complexes.Seminars in immunopathology · 2018Review
- Simultaneous exposure to FcγR and FcαR on monocytes and macrophages enhances antitumor activity in vivo.Oncotarget · 2017Article
- CD89-mediated recruitment of macrophages via a bispecific antibody enhances anti-tumor efficacy.OncoimmunologyArticle
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
Although IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, its etiology remains only partly understood. It is clear that the pathogenesis of IgAN involves the formation of macromolecular IgA1 complexes and increased levels of serum IgA1 and IgA1-immune complexes(IC), due to defective IgA1 clearance. Previous studies suggest that the blood and tissue myeloid cell-expressed IgA Fc receptor (FcαR/CD89) mediates IgA-IC clearance and its dysfunction, via decreased activity or excessive levels of soluble FcαR/sCD89 induces IgAN. Such a mechanism requires robust stimulation of IgAN levels via forced expression of CD89. In the absence of unequivocal evidence supporting such a mechanism to date, we attempted to test the extent of CD89-evoked IgAN by generating a transgenic mouse strain expressing human CD89 under the control of murine CD14 promotor. No deposition of IgA-CD89 complexes or glomerulonephritis was detected, however. Further studies showed that elimination of murine IgA was mediated by Kupffer cells. In patients, however, CD89/IgA complexes were detected, and injection of patient IgA induced IgAN-like features in CD89 Tg mice. In transgenic mice, IgAN pathogenesis involves impaired clearance of abnormal IgA via CD89, primarily by the Kupffer cells. Conditional IgAN progression in CD89 transgenic mice thus reveals important aspects of IgAN pathogenesis.
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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.