ArticleAmerican journal of respiratory cell and molecular biology2012
Indoleamine 2,3-dioxygenase and metabolites protect murine lung allografts and impair the calcium mobilization of T cells.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Decoding amino acid metabolism in hepatocellular carcinoma: critical nodes and novel therapeutic strategy.Frontiers in oncology · 2026Review
- Indoleamine-2,3-dioxygenase: An important controller in maintaining mesenchymal stem cell-mediated immunomodulatory homeostasis.Acta pharmaceutica Sinica. B · 2025Review
- GPX4 knockdown suppresses M2 macrophage polarization in gastric cancer by modulating kynurenine metabolism.Theranostics · 2025Article
- Amino acid metabolism reprogramming: shedding new light on T cell anti-tumor immunity.Journal of experimental & clinical cancer research : CR · 2023Review
- Immunomodulatory actions of a kynurenine-derived endogenous electrophile.Science advances · 2022Article
- Tryptophan Metabolism via Kynurenine Pathway: Role in Solid Organ Transplantation.International journal of molecular sciences · 2021Review
- Control of T-Cell Activation and Signaling by Amino-Acid Catabolizing Enzymes.Frontiers in cell and developmental biology · 2020Review
- Indoleamine 2,3-dioxygenase suppresses humoral alloimmunity via pathways that different to those associated with its effects on T cells.Biomedical reports · 2019Article
- Immunomodulatory Effects of Genetic Alterations Affecting the Kynurenine Pathway.Frontiers in immunology · 2019Review
- T Cell Calcium Signaling Regulation by the Co-Receptor CD5.International journal of molecular sciences · 2018Review
- Lymphatic Vessels: The Next Frontier in Lung Transplant.Annals of the American Thoracic Society · 2017Review
- Therapeutic lymphangiogenesis ameliorates established acute lung allograft rejection.The Journal of clinical investigation · 2015Article
- Prognostic significance of kynurenine 3-monooxygenase and effects on proliferation, migration, and invasion of human hepatocellular carcinoma.Scientific reports · 2015Article
- Endothelial indoleamine 2,3-dioxygenase protects against development of pulmonary hypertension.American journal of respiratory and critical care medicine · 2013Article
- Five-year update on the mouse model of orthotopic lung transplantation: Scientific uses, tricks of the trade, and tips for success.Journal of thoracic disease · 2012Article
- Mechanism Exploration on the Immunoregulation of Allogeneic Heart Transplantation Rejection in Rats With Exosome miRNA and Proteins From Overexpressed IDO1 BMSCs.Cell transplantationArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The enzyme indoleamine 2,3-dioxygenase (IDO) converts tryptophan into kynurenine metabolites that suppress effector T-cell function. In this study, we investigated IDO and its metabolite, 3-hydroxyanthranilic acid (3HAA), in regulating lung allograft rejection, using a murine orthotopic lung transplant model with a major mismatch (BALB/c donor and C57BL6 recipient). IDO was overexpressed in murine donor lungs, using an established nonviral (polyethylenimine carrier)-based gene transfer approach, whereas 3HAA was delivered daily via intraperitoneal injection. Increased IDO expression or its metabolite, 3HAA, resulted in a remarkable therapeutic effect with near normal lung function and little acute rejection, approximately A1, compared with A3 in untreated allografts (grading based on International Society for Heart and Lung Transplantation guidelines). We found that a high IDO environment for 7 days in lung allografts resulted in impaired T-cell activation, the production of multiple effector cytokines (IL-2, IL-4, IL-5, IL-6, IFN-γ, TNF-α, IL-12, and IL-13), and the generation of effector memory T cells (CD62L(lo)CD44(hi) phenotype). In isolated murine splenocytes, we observed that IDO/3HAA impaired T-cell receptor (TCR)-mediated T-cell activation, and more importantly, a decrease of intracellular calcium, phospholipase C-γ1 phosphorylation, and mitochondrial mass was evident. This work further illustrates the potential role of a high IDO environment in lung transplantation, and that the high IDO environment directly impairs TCR activation via the disruption of calcium signaling.
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Registered trials
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