ArticleEBioMedicine2023
The microbial metabolite desaminotyrosine enhances T-cell priming and cancer immunotherapy with immune checkpoint inhibitors.
Article in EBioMedicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Leveraging the bacteria for enhanced cancer immunotherapy: from a perspective of synthetic biology.Cancer biology & therapy · 2026Review
- Molecular pathways linking the gut microbiome to antitumor immunity.Trends in microbiology · 2026Review
- Article
- Regulation of PD-1PD-L1 Immune Checkpoints by Gut Microbiota Metabolites and Their Clinical Translational Research: A Review.Immunity, inflammation and disease · 2026Review
- Systematic verification of saliva-based biosignatures for oral cancer via targeted metabolomics.Journal of food and drug analysis · 2026Article
- The gut-tumor connection: the role of microbiota in cancer progression and treatment strategies.Journal of advanced research · 2026Review
- Article
- The potential of microbiome modulators to improve quality of life in cancer survivors through gut microbiome-immune interactions.Frontiers in molecular neuroscience · 2026Review
- The gut microbiome in colorectal cancer: molecular paradigms and translational frontiers.Frontiers in bioengineering and biotechnology · 2026Review
- Metabolism-Driven Modulation by the Human Microbiota: Implications for Cancer Therapy and Emerging Strategies.Advances in experimental medicine and biology · 2026Review
- The microbial metabolite desaminotyrosine is a potent antiobesity agent with potential effects on white adipose tissue remodeling in mice.Gut microbes · 2025Article
- The gut microbiota: an emerging modulator of drug resistance in hepatocellular carcinoma.Gut microbes · 2025Review
- Drug resistance in cancer: molecular mechanisms and emerging treatment strategies.Molecular biomedicine · 2025Review
- The microbial metabolite desaminotyrosine protects against graft-versus-host disease via mTORC1 and STING-dependent intestinal regeneration.Nature communications · 2025Article
- Metabolites as agents and targets for cancer immunotherapy.Nature reviews. Drug discovery · 2025Review
- Dietary Fiber Lacks a Consistent Effect on Immune Checkpoint Blockade Efficacy Across Diverse Murine Tumor Models.Cancer research · 2025Article
- The role of gut microbial metabolites in the T cell lifecycle.Nature immunology · 2025Review
- Microbiome dysbiosis and immune checkpoint inhibitors: Dual targets in Hepatocellular carcinoma management.World journal of hepatology · 2025Review
- Longitudinal analysis of gut microbiome and metabolome correlates of response and toxicity with idecabtagene vicleucel.Blood advances · 2025Article
- Faecalibacterium prausnitzii promotes anti-PD-L1 efficacy in natural killer/T-cell lymphoma by enhancing antitumor immunity.BMC medicine · 2025Article
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Authors and funding
15 authors.
Funding
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Abstract
backgroundInter-individual differences in response to immune checkpoint inhibitors (ICI) remain a major challenge in cancer treatment. The composition of the gut microbiome has been associated with differential ICI outcome, but the underlying molecular mechanisms remain unclear, and therapeutic modulation challenging.
methodsWe established an in vivo model to treat C57Bl/6j mice with the type-I interferon (IFN-I)-modulating, bacterial-derived metabolite desaminotyrosine (DAT) to improve ICI therapy. Broad spectrum antibiotics were used to mimic gut microbial dysbiosis and associated ICI resistance. We utilized genetic mouse models to address the role of host IFN-I in DAT-modulated antitumour immunity. Changes in gut microbiota were assessed using 16S-rRNA sequencing analyses.
findingsWe found that oral supplementation of mice with the microbial metabolite DAT delays tumour growth and promotes ICI immunotherapy with anti-CTLA-4 or anti-PD-1. DAT-enhanced antitumour immunity was associated with more activated T cells and natural killer cells in the tumour microenvironment and was dependent on host IFN-I signalling. Consistent with this, DAT potently enhanced expansion of antigen-specific T cells following vaccination with an IFN-I-inducing adjuvant. DAT supplementation in mice compensated for the negative effects of broad-spectrum antibiotic-induced dysbiosis on anti-CTLA-4-mediated antitumour immunity. Oral administration of DAT altered the gut microbial composition in mice with increased abundance of bacterial taxa that are associated with beneficial response to ICI immunotherapy.
interpretationWe introduce the therapeutic use of an IFN-I-modulating bacterial-derived metabolite to overcome resistance to ICI. This approach is a promising strategy particularly for patients with a history of broad-spectrum antibiotic use and associated loss of gut microbial diversity.
fundingMelanoma Research Alliance, Deutsche Forschungsgemeinschaft, German Cancer Aid, Wilhelm Sander Foundation, Novartis Foundation.
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