ArticleAdvanced healthcare materials2025
Short-Chain Fatty Acids Modulate Anti-ROR1 CAR T-Cell Function and Exhaustion in an Intestinal Adenocarcinoma-on-Chip Model.
Article in Advanced healthcare materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed.
- Short-chain fatty acids act as metabolic and epigenetic regulators in CAR T cell therapy.Molecular therapy. Oncology · 2026Review
- The Gut-Pancreas Axis in Type 1 Diabetes: Emerging Insights into Microbiota and Immune Interactions.International journal of molecular sciences · 2026Review
- Metabolic reprogramming of CAR-T cells: a multi-pronged strategy to conquer the immunosuppressive tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- Modeling Clostridioides difficile toxin pathogenesis and antiserum protection in an immunocompetent intestine-on-chip platform.Scientific reports · 2026Article
- Short-chain fatty acids in the tumor microenvironment: from molecular mechanisms to cancer therapy.Theranostics · 2026Review
- Post-Translational Modifications in Cancer-Associated CD8⁺ T-Cell Exhaustion: Mechanisms and Therapeutic Opportunities.International journal of biological sciences · 2026Review
- Gut microbial metabolites in cancer immunomodulation.Molecular cancer · 2025Review
- Hexanoic Acid Intake Enhances Anti-Tumor Immune Responses in Colorectal Cancer by Reducing the Immunosuppressive Function of Tregs.Molecular nutrition & food research · 2025Article
- Short-Chain Fatty Acids Modulate Anti-ROR1 CAR T-Cell Function and Exhaustion in an Intestinal Adenocarcinoma-on-Chip Model.Advanced healthcare materials · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Chimeric antigen receptor (CAR) T-cell therapy represents a promising approach for cancer treatment, with receptor tyrosine kinase-like orphan receptor 1 (ROR1) emerging as a novel target in malignancies. This study investigates how short-chain fatty acids (SCFAs), key microbiota-derived metabolites, modulate anti-ROR1 CAR T-cell efficacy using a physiologically relevant intestinal adenocarcinoma-on-chip model that replicates the human intestinal microenvironment. The findings demonstrate that propionate and butyrate inhibit anti-ROR1 CAR T-cell function by reducing infiltration, cytotoxicity, and cytokine release while preserving junctional integrity within the tumor model. Mechanistically, these SCFAs inhibit histone deacetylase activity and promote a phenotype switch toward regulatory T-cells, as indicated by increased expression of FoxP3 and RORγt. Additionally, propionate and butyrate upregulate PD-1 and TIM-3, markers of T-cell exhaustion and immune tolerance, and induce a dose- and time-dependent reduction in proinflammatory cytokines. In contrast, acetate and pentanoate promote a proinflammatory T helper 17 phenotype. These results highlight the immunomodulatory effects of SCFAs on CAR T-cell function, emphasizing the need to consider microbiota-derived metabolites in CAR T-cell therapies.
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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.