However, the mechanism responsible for the anti-tumor activity of IL-17 was different from that reported by Wakita and involved a reciprocal activatory interaction between the γδ17 cells and MDSC, which was mediated by cancer cells: in detail, γδ T cell-derived IL-17 induced CXCL5 production by tumor cells, which in turn recruited MDSC to the tumor sites via CXCL5/CXCR2-interaction. Here, CXCR2 is linked to neoplasm.