ArticleJCI insight2024
Indoleamine-2,3-dioxygenase inhibition improves immunity and is safe for concurrent use with cART during Mtb/SIV coinfection.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed.
- Early immune dysregulation iniScience · 2026Article
- The Kynurenine Pathway in Tuberculosis: Focus on Immunometabolic Regulation, Compartment-Specific Biology, and Therapeutic Potential.Life (Basel, Switzerland) · 2026Review
- Targeting Tryptophan Metabolism for Tuberculosis Biomarkers and Host-Directed Therapy.The Journal of infectious diseases · 2026Review
- Using Imaris to rigorously track PET-defined sites of lung inflammation inAmerican journal of diagnostic imaging · 2026Article
- Concurrent TB and HIV therapies control TB reactivation during co-infection but not chronic immune activation.Nature communications · 2025Article
- Development and preclinical evaluation of next-generation ΔsigH-based live candidate vaccines.JCI insight · 2025Article
- Advances in host-directed therapy for tuberculosis and HIV coinfection: enhancing immune responses.Trends in microbiology · 2025Review
- Effect of anti-CD4 mAb induced by inhibiting B cell disorder on immune reconstruction of HIV-infected immunological non-responders.Molecular medicine (Cambridge, Mass.) · 2025Article
- Dissecting inflammation in the immunemetabolomic era.Cellular and molecular life sciences : CMLS · 2025Review
- Driving innovation from discovery to access: Meeting report of the 7Gates open research · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Chronic immune activation promotes tuberculosis (TB) reactivation in the macaque Mycobacterium tuberculosis (M. tuberculosis)/SIV coinfection model. Initiating combinatorial antiretroviral therapy (cART) early lowers the risk of TB reactivation, but immune activation persists. Studies of host-directed therapeutics (HDTs) that mitigate immune activation are, therefore, required. Indoleamine 2,3, dioxygenase (IDO), a potent immunosuppressor, is one of the most abundantly induced proteins in NHP and human TB granulomas. Inhibition of IDO improves immune responses in the lung, leading to better control of TB, including adjunctive to TB chemotherapy. The IDO inhibitor D-1 methyl tryptophan (D1MT) is, therefore, a bona fide TB HDT candidate. Since HDTs against TB are likely to be deployed in an HIV coinfection setting, we studied the effect of IDO inhibition in M. tuberculosis/SIV coinfection, adjunctive to cART. D1MT is safe in this setting, does not interfere with viral suppression, and improves the quality of CD4+ and CD8+ T cell responses, including reconstitution, activation and M. tuberculosis-specific cytokine production, and access of CD8+ T cells to the lung granulomas; it reduces granuloma size and necrosis, type I IFN expression, and the recruitment of inflammatory IDO+ interstitial macrophages (IMs). Thus, trials evaluating the potential of IDO inhibition as HDT in the setting of cART in M. tuberculosis/HIV coinfected individuals are warranted.
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