ArticleJournal of nephrology2014
Suppression of experimental autoimmune glomerulonephritis by tryptophan.
Article in Journal of nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 11 citations in OpenAlex.
- 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
- Kynurenine Pathway after Kidney Transplantation: Friend or Foe?International journal of molecular sciences · 2024Review
- Kynurenine pathway in kidney diseases.Pharmacological reports : PR · 2022Review
- The Kynurenine Pathway in Acute Kidney Injury and Chronic Kidney Disease.American journal of nephrology · 2021Review
- Bone Marrow Mesenchymal Stem Cells Alleviate Extracellular Kynurenine Levels, as Detected by High-Performance Liquid Chromatography.Inflammation · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIndoleamine 2, 3-dioxygenase (IDO), a heme-containing dioxygenase, can catalyze tryptophan degradation and produce a local microenvironment with tryptophan depletion and tryptophan metabolites accumulation, which may suppress T cell-mediated immunity and play an important immunosuppressive role in many diseases. Previous studies suggested that tryptophan depletion is an important immunosuppressive mechanism of IDO, while recent evidence shows that tryptophan metabolites may also be useful for inducing the T cell immune tolerance. However, it remains unclear whether tryptophan catabolites play a protective role in anti-glomerular basement membrane (anti-GBM) glomerulonephritis (GN), which is a type 1 T-helper (Th1)-mediated autoimmune disease.
methodsWe examined the effect of tryptophan catabolites, 3-hydroxykynurenine acid and 3-hydroxyanthranilic acid, on renal injury in experimental autoimmune glomerulonephritis (EAG) of Wistar-Kyoto rats and explored their protective mechanism.
resultsTreatment by either 3-hydroxyanthranilic acid or 3-hydroxykynurenic acid attenuated the kidney disease of EAG rats, with decreased glomerular histological injury and inflammatory cell infiltration, lightened urinary protein, and improved renal function compared to phosphate buffered saline-treated EAG rats. This was associated with significantly increased apoptosis and decreased proliferation of splenic activated T cells in vivo, inducing the deviation of cytokines of antigen-special T cells from Th1 to Th2.
conclusionsTryptophan metabolites play an important immunosuppressive role in the development of anti-GBM GN and might offer a new strategy for treating this disease.
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