Figure 1.

Abnormal tumor angiogenesis promotes tumor immune evasion. (A) Wide gaps between endothelial cells, detached pericytes, and thick/thin basement membranes, together with high levels of VEGF and low expression of endothelial adhesion molecules, reduce adhesion, extravasation, and infiltration of leukocytes into the tumor bed and contribute to establish the immune-desert and immune-excluded BC phenotype. (B) Ability of TME to promote the release of VEGF, other angiogenic factors, and protumor cytokines capable of inhibiting the maturation and function of DCs (characterized by low expression of CD80, CD83, CD86, etc.). (C) The exhaustion state of T cells is directly induced by the binding between the VEGF-R receptor and the VEGF-A ligand, major source of the inhibition of their effector function. (D) Vascular microenvironment produces multiple cytokines that recall immunosuppressive cells such as TAM2, Treg, and MDSC and reduce tumor infiltration and activity of DC, NK, and T cells. The figure was created with BioRender.com.