ArticleCellular & molecular immunology2024
Kynurenine-AhR reduces T-cell infiltration and induces a delayed T-cell immune response by suppressing the STAT1-CXCL9/CXCL10 axis in tuberculosis.
Article in Cellular & molecular immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Gut microbiota metabolites in the immunoregulation of enteritis: research progress.Frontiers in immunology · 2025Pooled it
- The gut microbiota-tryptophan metabolism-immune axis in inflammatory bowel disease: Mechanisms and therapeutic prospects.Human vaccines & immunotherapeutics · 2026Review
- Genetic and immunologic determinants of BCG disease: from mechanism to prevention.Annals of medicine · 2026Review
- Positive feedback loop via HIF-1α lactylation driven by kynurenine promotes glycolysis.Oncogene · 2026Article
- Tryptophan metabolism in tumor microenvironment and therapeutic implications.Journal of advanced research · 2026Review
- 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
- Emerging insights into CC and CXC chemokines and their receptors in Mycobacterium tuberculosis infection.FEBS open bio · 2026Review
- The Therapeutic Effect of Tapinarof on In Vitro Cutaneous Lupus-like Keratinocyte Model.International journal of molecular sciences · 2026Article
- T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- HowVaccines · 2026Review
- Enhanced tuberculosis control via leveraging dendritic cell-mediated Th1 responses in preventive and immunotherapeutic vaccine strategies.Journal of advanced research · 2026Article
- Gut-microbiota-derived 3-indoleacrylic acid alleviates neonatal necrotizing enterocolitis by inhibiting epithelial necroptosis.Cell reports. Medicine · 2026Article
- Not so cold after all: tumor infiltrating CD8+ T cells in EBV-positive Burkitt lymphoma are quiescent, not exhausted.bioRxiv : the preprint server for biology · 2026Article
- Two orthobunyaviruses: OYAV and EBIV co-opt the AhR-CYP1A1 axis to suppress type I interferon responses.Virologica Sinica · 2026Article
- Targeting Tryptophan Metabolism for Tuberculosis Biomarkers and Host-Directed Therapy.The Journal of infectious diseases · 2026Review
- Metabolic characterization of tumor-immune interactions by multiplexed immunofluorescence reveals spatial mechanisms of immunotherapy response in non-small cell lung carcinoma (NSCLC).Nature communications · 2026Article
- Tumor Cells as Architects of Immune Refractoriness: Dismantling Intrinsic Programs of Tumor Cells for Clinical Translation.Immune network · 2026Review
- Tryptophan and polyamine metabolism dysregulation serves as an early marker of high-fat diet-induced glucose intolerance.Journal of lipid research · 2026Article
- Insights into the host response to 'dormant' Mycobacterium tuberculosis utilizing 'Vitamin C-induced dormant Mtb' THP-1 cell infection model.BMC genomics · 2026Article
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9 authors.
Funding
Abstract
Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), is a critical global health issue that is complicated by the ability of the pathogen to delay the host's T-cell immune response. This delay in T-cell recruitment to the site of infection is a pivotal survival strategy for Mtb, allowing it to establish a persistent chronic infection. To investigate the underlying mechanisms, this study focused on Mtb's exploitation of host tryptophan metabolism. Mtb upregulates indoleamine 2,3-dioxygenase 1 (IDO1) in inflammatory macrophages, thereby increasing kynurenine (Kyn) production. Kyn then activates the aryl hydrocarbon receptor (AhR), leading to the upregulation of suppressor of cytokine signaling 3 and subsequent inhibition of the JAK-STAT1 signaling pathway. This results in reduced secretion of the chemokines CXCL9 and CXCL10, which are crucial for T-cell recruitment to the lungs. Supported by in vivo mouse models, our findings reveal that disrupting this pathway through AhR knockout significantly enhances T-cell infiltration and activity, thereby undermining Mtb-induced immunosuppression. In contrast, additional Kyn injection obviously inhibited T-cell infiltration and activity. These results highlight potential therapeutic targets of AhR and IDO1, offering new avenues for enhancing the host immune response against tuberculosis and guiding future vaccine development efforts.
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