The role of the IL-23/IL-17A axis in tumor-immune interactions is a matter of controversy. While some suggest that IL-17A producing T cells (TH17) can suppress tumor growth, others report that IL-17A and IL-23 accelerate tumor growth. Here, we systematically assessed the impact of IL-17A-secreting lymphocytes in several murine models of tumor lung metastasis. Genetic fate-mapping revealed that IL-17A was secreted within lung metastases predominantly by γδ T cells, while TH17 cells were virtually absent. Using different tumor models, we found Il17a-/- mice to consistently develop fewer pulmonary tumor colonies. IL-17A specifically increased blood vessel permeability and the expression of E-selectin and VCAM-1 by lung endothelial cells in vivo. In transgenic mice, specific targeting of IL-17A to the endothelium increased the number of tumor foci. Moreover, the direct impact of IL-17A on lung endothelial cells resulted in impaired endothelial barrier integrity showing that IL-17A promotes the formation of lung metastases through tumor-endothelial transmigration.