Aim <p>The primary goal of this research is to gain a deeper understanding of the intricate role that VEGF plays in creating an immunologically tolerant milieu in cases of OSCC or oral squamous cell carcinoma. Examining how VEGF affects the behavior and functionality of dendritic cells (DCs). Through an examination of the interactions among VEGF, DCs, and the tumor microenvironment.</p> Methods <p>This study investigated the expression of the immunosuppressive markers IDO and programmed cell death ligand 1 (PD-L1) in DCs under the effect of VEGF employing real-time PCR (RT-PCR), flow cytometry and Western blot (WB). Additionally, mixed lymphocyte reactions and tumor cell cytotoxicity assays were conducted to assess functional changes in DCs.</p> Results <p>VEGF exposure led to an upregulation of IDO and PD-L1 in DCs, coupled with reduced T-cell proliferation and altered immune responses in the tumor microenvironment. In vivo studies using mice models further substantiated the role of VEGF in enhancing tumor immune tolerance.</p> Conclusion <p>Our findings elucidate the crucial role of VEGF in OSCC progression by modulating DC function, offering new insights into potential immunotherapeutic strategies targeting VEGF-mediated pathways.</p>

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The impact of vascular endothelial growth factor on oral squamous cell carcinoma through dendritic cell induction and facilitation of tumor immune tolerance

  • Peng Zhang,
  • Yue Xu,
  • Bolei Cai,
  • Jiaqiang Xu,
  • Tao Wang,
  • Hongyan Xu

摘要

Aim

The primary goal of this research is to gain a deeper understanding of the intricate role that VEGF plays in creating an immunologically tolerant milieu in cases of OSCC or oral squamous cell carcinoma. Examining how VEGF affects the behavior and functionality of dendritic cells (DCs). Through an examination of the interactions among VEGF, DCs, and the tumor microenvironment.

Methods

This study investigated the expression of the immunosuppressive markers IDO and programmed cell death ligand 1 (PD-L1) in DCs under the effect of VEGF employing real-time PCR (RT-PCR), flow cytometry and Western blot (WB). Additionally, mixed lymphocyte reactions and tumor cell cytotoxicity assays were conducted to assess functional changes in DCs.

Results

VEGF exposure led to an upregulation of IDO and PD-L1 in DCs, coupled with reduced T-cell proliferation and altered immune responses in the tumor microenvironment. In vivo studies using mice models further substantiated the role of VEGF in enhancing tumor immune tolerance.

Conclusion

Our findings elucidate the crucial role of VEGF in OSCC progression by modulating DC function, offering new insights into potential immunotherapeutic strategies targeting VEGF-mediated pathways.