Figure 1.

Illustration of proposed mechanism for combination therapy with anti-vascular endothelial growth factor (VEGF)/VEGFR2 and immune checkpoint blockade (ICB). On the left: tumor with abnormal vessels, characterized by a defective structure, poor pericyte coverage, areas of hypoxia and impaired T cell infiltration. On the right: tumor after antiangiogenic therapy with a normalized vasculature; enhanced pericyte coverage, expression of adhesion molecules and increased T cell infiltration. The formation of HEVs leads to more efficient T cell influx into tumors. IFNy-mediated expression of immune inhibitory checkpoint molecules, such as PD-L1, can be counteracted by the use of ICB promoting more efficient tumor control.