ArticleInternational urology and nephrology2020
The therapeutic effect of dendritic cells expressing indoleamine 2,3-dioxygenase (IDO) on an IgA nephropathy mouse model.
Article in International urology and nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Plasmacytoid dendritic cells modulate the production of mucosal IgA in IgA nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026Article
- Review
- Cancer-associated fibroblast-mediated immune evasion: molecular mechanisms of stromal-immune crosstalk in the tumor microenvironment.Frontiers in immunology · 2025Review
- Regulatory cell therapy for kidney transplantation and autoimmune kidney diseases.Pediatric nephrology (Berlin, Germany) · 2025Review
- Identification of key necroptosis-related genes and immune landscape in patients with immunoglobulin A nephropathy.BMC nephrology · 2024Article
- Prediction Model for Early-Stage CKD Using the Naples Prognostic Score and Plasma Indoleamine 2,3-dioxygenase Activity.Journal of inflammation research · 2024Article
- Plasma Tryptophan-Kynurenine Pathway Metabolites and Risk for Progression to End-Stage Kidney Disease in Patients With Type 2 Diabetes.Diabetes care · 2023Article
- Tolerogenic dendritic cells in type 1 diabetes: no longer a concept.Frontiers in immunology · 2023Review
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- The PDE4 inhibitor tanimilast shows distinct immunomodulatory properties associated with a type 2 endotype and CD141 upregulation.Journal of translational medicine · 2022Article
- The Footprint of Kynurenine Pathway in Cardiovascular Diseases.International journal of tryptophan research : IJTR · 2022Review
- The Kynurenine Pathway in Acute Kidney Injury and Chronic Kidney Disease.American journal of nephrology · 2021Review
- T lymphocytes in IgA nephropathy.Experimental and therapeutic medicine · 2020Article
- Intestinal Bacteria Encapsulated by Biomaterials Enhance Immunotherapy.Frontiers in immunology · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveIgA nephropathy (IgAN) is one of the most common glomerulonephritis in the world, especially in Asian population. IgAN usually progresses slowly, but it is still an important cause of chronic renal failure. IgAN is characterized by abnormal increase of IgA1 level and deposition in mesangium. At present, there is no specific treatment. MATERIALS AND
methodsPrevious reports have shown that DC cells expressing immunosuppressive factors can significantly reduce the symptoms of arthritis in arthritis models. Indoleamine 2,3-dioxygenase (IDO) is an important tryptophan degrading enzyme and an important factor regulating immunotolerance. DC expressing functional IDO can inhibit effector T cells by consuming essential tryptophan and/or producing toxic metabolites and promoting the differentiation of Treg cells, which exhibits immunosuppressive effect. In this study, we constructed a IgAN mouse model. The mature DC cells overexpressing IDO were induced in vitro and transfused back to IgAN mice to observe their effects on inflammation and renal injury.
resultsThe results showed that overexpression of IDO did not affect the maturation of DC cells. The proportion of CD3 + CD4 + and CD3 + CD8 + cells decreased significantly and the proportion of CD4 + CD25 + Foxp3 + cells increased significantly in kidney tissue of IgAN mice after the reinfusion of IDO-expressing DC. The contents of IL-2, IL-4, IL-6, and IL-17A in kidney tissue of IgAN mice also decreased significantly, the damage of kidney tissue was alleviated, ACR was decreased, collagen fibre content in kidney tissue was decreased, and IgA deposition in glomerular mesangium was decreased in IgAN mice.
conclusionsIt has the potential to treat IgAN by upregulating the expression of IDO in DC cells by genetic engineering and reinfusion into vivo.
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