ArticleClinical and experimental immunology2009
Inhibition of indoleamine 2, 3-dioxygenase-mediated tryptophan catabolism accelerates crescentic glomerulonephritis.
Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Integrative Pharmacokinetic and Metabolomic Profiling ofInternational journal of molecular sciences · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Investigation of the Impact of Tryptophan-Metabolizing Enzymes and Kynurenic Acid on Antibody-Mediated Glomerulonephritis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Time course profiling of the kynurenine pathway activity in a pig model of crescentic glomerulonephritis.BMC nephrology · 2025Article
- The role of the kynurenine pathway in cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- Plasma Tryptophan-Kynurenine Pathway Metabolites and Risk for Progression to End-Stage Kidney Disease in Patients With Type 2 Diabetes.Diabetes care · 2023Article
- Identification of Genetic Markers Linked to The Activity of Indoleamine 2,3-Dioxygenase and Kidney Function.Metabolites · 2023Article
- Kynurenine pathway in kidney diseases.Pharmacological reports : PR · 2022Review
- Kidney organoid systems for studies of immune-mediated kidney diseases: challenges and opportunities.Cell and tissue research · 2021Review
- The Kynurenine Pathway in Acute Kidney Injury and Chronic Kidney Disease.American journal of nephrology · 2021Review
- Correlation of Indoleamine-2,3-Dioxygenase and Chronic Kidney Disease: A Pilot Study.Journal of immunology research · 2021Observational
- Limited Effect of Indolamine 2,3-Dioxygenase Expression and Enzymatic Activity on Lupus-Like Disease in B6.Nba2 Mice.Frontiers in immunology · 2019Article
- Indoleamine 2, 3-dioxygenase (IDO) increases during renal fibrogenesis and its inhibition potentiates TGF-β 1-induced epithelial to mesenchymal transition.BMC nephrology · 2017Article
- Amino acid metabolism inhibits antibody-driven kidney injury by inducing autophagy.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Human renal tubular epithelial cells suppress alloreactive T cell proliferation.Clinical and experimental immunology · 2015Article
- The Mechanisms of Human Renal Epithelial Cell Modulation of Autologous Dendritic Cell Phenotype and Function.PloS one · 2015Article
- Suppression of experimental autoimmune glomerulonephritis by tryptophan.Journal of nephrology · 2014Article
- High activity of indoleamine 2,3-dioxygenase is associated with renal insufficiency in Puumala hantavirus induced nephropathia epidemica.Journal of medical virology · 2011Article
- Suppression of humoral immune response to hepatitis B surface antigen vaccine in BALB/c mice by 1-methyl-tryptophan co-administration.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2011Article
- TNFα mediates stress-induced depression by upregulating indoleamine 2,3-dioxygenase in a mouse model of unpredictable chronic mild stress.European cytokine networkArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunomodulatory enzyme indoleamine 2, 3-dioxygenase (IDO) is one of the initial and rate-limiting enzymes involved in the catabolism of the essential amino acid tryptophan. Via catalysing tryptophan degradation, IDO suppresses adaptive T cell-mediated immunity and plays an important role in various forms of immune tolerance. Its role in T helper type 1 (Th1)-directed, cell-mediated crescentic glomerulonephritis (GN) is still unclear. Therefore, we investigated the activity and role of IDO in crescentic GN using a model of nephrotoxic serum nephritis (NTN), and IDO activity was inhibited by 1-methyl-tryptophan (1-MT) in vivo. Our results showed that activity of IDO, as determined by high performance liquid chromatography analysis of the kynurenine/tryptophan ratio, was increased markedly in the serum and renal tissue of NTN mice, and immunohistochemistry revealed that expression of IDO was up-regulated significantly in glomeruli and renal tubular epithelial cells during NTN. Treatment with 1-MT resulted in significantly exacerbated kidney disease with increased glomerular crescent formation, accumulation of CD4(+)T cells and macrophages in renal tissue, and augmented renal injury compared with phosphate-buffered saline-treated NTN mice, which was associated with enhanced Th1 responses and intrarenal cellular proliferation. These findings suggest that the development of NTN was regulated negatively by increased IDO activity, and IDO might play an important role in the pathogenesis of crescentic GN.
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