High-Fat Diet Promotes Tumor Immune Evasion via CD155 Upregulation in Colorectal Cancer.
1/5 보강
[BACKGROUND] Obesity-induced metabolic stress impairs the efficacy of immune checkpoint blockade (ICB) therapy, but the mechanisms linking a high-fat diet (HFD) to immune suppression remain unclear.
APA
Liu L, Mo L, et al. (2026). High-Fat Diet Promotes Tumor Immune Evasion via CD155 Upregulation in Colorectal Cancer.. Immunological investigations, 55(2), 290-308. https://doi.org/10.1080/08820139.2025.2600597
MLA
Liu L, et al.. "High-Fat Diet Promotes Tumor Immune Evasion via CD155 Upregulation in Colorectal Cancer.." Immunological investigations, vol. 55, no. 2, 2026, pp. 290-308.
PMID
41420878
Abstract
[BACKGROUND] Obesity-induced metabolic stress impairs the efficacy of immune checkpoint blockade (ICB) therapy, but the mechanisms linking a high-fat diet (HFD) to immune suppression remain unclear.
[OBJECTIVE] To investigate how HFD-induced metabolic changes modulate the tumor immune microenvironment through the STAT3/CD155 axis.
[METHODS] Murine colorectal cancer models using control, CD155-overexpressing (CD155 OE), and STAT3 knockdown CT26 cells were established under normal or HFD conditions with anti - PD-L1 treatment. Tumor growth, immune infiltration, and gene expression were analyzed by flow cytometry, Western blotting, and chromatin immunoprecipitation.
[RESULTS] HFD impaired anti - PD-L1 efficacy and accelerated tumor growth. Mechanistically, HFD promoted STAT3 nuclear translocation and CD155 upregulation, reducing CD8 T cell infiltration and enhancing regulatory T cell accumulation. Chromatin immunoprecipitation confirmed direct STAT3 binding to the CD155 promoter, while STAT3 knockdown reversed these effects and restored antitumor immunity in HFD-fed mice.
[CONCLUSION] HFD-induced metabolic stress drives immune evasion via the STAT3/CD155 axis. Targeting this pathway may improve ICB efficacy in obesity-related cancers.
[OBJECTIVE] To investigate how HFD-induced metabolic changes modulate the tumor immune microenvironment through the STAT3/CD155 axis.
[METHODS] Murine colorectal cancer models using control, CD155-overexpressing (CD155 OE), and STAT3 knockdown CT26 cells were established under normal or HFD conditions with anti - PD-L1 treatment. Tumor growth, immune infiltration, and gene expression were analyzed by flow cytometry, Western blotting, and chromatin immunoprecipitation.
[RESULTS] HFD impaired anti - PD-L1 efficacy and accelerated tumor growth. Mechanistically, HFD promoted STAT3 nuclear translocation and CD155 upregulation, reducing CD8 T cell infiltration and enhancing regulatory T cell accumulation. Chromatin immunoprecipitation confirmed direct STAT3 binding to the CD155 promoter, while STAT3 knockdown reversed these effects and restored antitumor immunity in HFD-fed mice.
[CONCLUSION] HFD-induced metabolic stress drives immune evasion via the STAT3/CD155 axis. Targeting this pathway may improve ICB efficacy in obesity-related cancers.
MeSH Terms
Animals; Colorectal Neoplasms; Diet, High-Fat; Mice; STAT3 Transcription Factor; Up-Regulation; Tumor Escape; Tumor Microenvironment; Cell Line, Tumor; Receptors, Virus; Humans; Gene Expression Regulation, Neoplastic; Disease Models, Animal; CD8-Positive T-Lymphocytes; B7-H1 Antigen; Lymphocytes, Tumor-Infiltrating; Male
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