VEGFA/VEGFR2-targeted therapies prevent the VEGFA-induced proliferation of regulatory T cells in cancer

Magali Terme, Eric Tartour, Julien Taieb, Magali Terme, Eric Tartour, Julien Taieb

Abstract

Some of the anti-angiogenic agents currently used to treat solid malignancies have effects on tumor endothelial cells as well as on immune cells. We have recently demonstrated that targeting the vascular endothelial growth factor A (VEGFA)/VEGF receptor 2 (VEGFR2) signaling pathway reduces the proportion of regulatory T cells (Treg) in a mouse model of colorectal cancer (CRC) and in metastatic CRC patients as it inhibits tumor-induced Treg proliferation.

Keywords: VEGF-A; colorectal cancer; immunosuppression; proliferation; regulatory T cells; tumor.

Figures

https://www.ncbi.nlm.nih.gov/pmc/articles/instance/3782524/bin/onci-2-e25156-g1.jpg
Figure 1. Impact of VEGFA/VEGFR-targeted therapeutics on tumor-induced immunosuppression. Tumor-derived vascular endothelial growth factor A (VEGFA) can block the maturation of dendritic cells (DCs) and induce the expansion of myeloid-derived suppressor cells. Immature DCs as well as MDSCs favor the generation of regulatory T cells (Tregs). VEGFA can also induce the proliferation of VEGF receptor 2 (VEGFR2)+ Tregs. VEGFA/VEGFR-targeted therapies can exert antineoplastic effects by interfering with all these mechanisms.

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Source: PubMed

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