ArticleJournal for immunotherapy of cancer2025
CPT1A inhibition alleviates plasmacytoid dendritic cell-mediated immune suppression in colon cancer through fatty acid oxidation modulation.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Article
- Engineered Xenogeneic Bone Scaffold with IL-10 Nanodelivery System: Immunomodulation and BMSC Fate Programming for Skull Defect Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- The emerging metabolic role and treatment target of CPT1A in CRC.Frontiers in cell and developmental biology · 2026Review
- Immunosuppressive cells as barriers to cancer therapy: mechanisms and emerging solutions.Frontiers in immunology · 2026Review
- The metabolism-immune axis in colorectal cancer: remodeling the tumor microenvironment through metabolite signaling.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe tolerization of plasmacytoid dendritic cells (pDCs) within the tumor microenvironment facilitates immune evasion, thereby significantly limiting the efficacy of cancer immunotherapy. Metabolic regulators are crucial in determining immune cell fate. However, the specific metabolic modifications influencing tumor-associated pDCs (TA-pDCs) are largely uncharacterized.
methodsWe isolated TA-pDCs from patients with colon cancer and mouse models for RNA sequencing detection and immunofluorescence staining. Further, in vitro and in vivo models of colon cancer were used to explore the underlying mechanisms of the fatty acid oxidation (FAO) regulatory pathway of TA-pDCs and its immunosuppressive function.
resultsPeroxisome proliferator-activated receptor gamma pathway promotes FAO in TA-pDCs by upregulating the expression of carnitine palmitoyltransferase-1A (CPT1A). The inhibition of CPT1A significantly reduced the immunosuppressive checkpoint inducible co-stimulator ligand (ICOSL) and increased the levels of the immune-activating protein OX40L and pro-inflammatory cytokines interferon-α and tumor necrosis factor-α. These alterations enhanced CD8
conclusionsThese findings elucidate the molecular mechanism of CPT1A-mediated FAO in TA-pDCs and its implications in immune evasion, suggesting a novel therapeutic strategy for colon cancer immunotherapy.
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