ArticlePloS one2012
M. tuberculosis induces potent activation of IDO-1, but this is not essential for the immunological control of infection.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- Tryptophan and Its Derived Metabolites as Biomarkers for Tuberculosis Disease: A Systematic ReviewIranian biomedical journal · 2024Pooled it
- Tryptophan catabolism reflects disease activity in human tuberculosis.JCI insight · 2020Trial
- Interferon-driven alterations of the host's amino acid metabolism in the pathogenesis of typhoid fever.The Journal of experimental medicine · 2016Trial
- The Kynurenine Pathway in Tuberculosis: Focus on Immunometabolic Regulation, Compartment-Specific Biology, and Therapeutic Potential.Life (Basel, Switzerland) · 2026Review
- Pathogenesis of Tuberculosis: Interplay Between Host Antituberculosis Immunity and Immune Evasion Strategies ofMedComm · 2026Review
- The immunometabolic topography of cellular organization and bacterial control in tuberculosis granulomas.Nature immunology · 2026Article
- Interleukin-1 receptor antagonist is a conserved early factor for exacerbating tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2025Article
- Review
- Metabolic insights into HIV/TB co-infection: an untargeted urinary metabolomics approach.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- Immune mechanisms of granuloma formation in sarcoidosis and tuberculosis.The Journal of clinical investigation · 2024Review
- New insight into arginine and tryptophan metabolism in macrophage activation during tuberculosis.Frontiers in immunology · 2024Review
- Kynurenine Pathway in Respiratory Diseases.International journal of tryptophan research : IJTR · 2024Review
- Recombinant Human Bone Morphogenetic Protein-2 Priming of Mesenchymal Stem Cells Ameliorate Acute Lung Injury by Inducing Regulatory T Cells.Immune network · 2023Article
- Immune Responses in Lung Granulomas during Mtb/HIV Co-Infection: Implications for Pathogenesis and Therapy.Pathogens (Basel, Switzerland) · 2023Review
- Inhibition of indoleamine dioxygenase leads to better control of tuberculosis adjunctive to chemotherapy.JCI insight · 2023Article
- The Kynurenine/Tryptophan Ratio as a Promising Metabolomic Biomarker for Diagnosing the Spectrum of Tuberculosis Infection and Disease.International journal of general medicine · 2023Review
- Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023Review
- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
- Mesenchymal-epithelial Transition Factor Regulates Monocyte Function during Mycobacterial Infection via Indoleamine 2,3-dioxygenase.Current medical science · 2022Article
- Single-nucleotide polymorphisms and activities of indoleamine 2,3-dioxygenase isoforms, IDO1 and IDO2, in tuberculosis patients.Hereditas · 2022Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Indoleamine 2,3-dioxygenesae-1 (IDO-1) catalyses the initial, rate-limiting step in tryptophan metabolism, thereby regulating tryptophan availability and the formation of downstream metabolites, including picolinic and quinolinic acid. We found that Mycobacterium tuberculosis infection induced marked upregulation of IDO-1 expression in both human and murine macrophages in vitro and in the lungs of mice following aerosol challenge with M. tuberculosis. The absence of IDO-1 in dendritic cells enhanced the activation of mycobacteria-specific T cells in vitro. Interestingly, IDO-1-deficiency during M. tuberculosis infection in mice was not associated with altered mycobacteria-specific T cell responses in vivo. The bacterial burden of infected organs, pulmonary inflammatory responses, and survival were also comparable in M. tuberculosis-infected IDO-1 deficient and wild type animals. Tryptophan is metabolised into either picolinic acid or quinolinic acid, but only picolinic acid inhibited the growth of M. tuberculosis in vitro. By contrast macrophages infected with pathogenic mycobacteria, produced quinolinic, rather than picolinic acid, which did not reduce M. tuberculosis growth in vitro. Therefore, although M. tuberculosis induces robust expression of IDO-1 and activation of tryptophan metabolism, IDO-1-deficiency fails to impact on the immune control and the outcome of the infection in the mouse model of tuberculosis.
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Registered trials
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.