The mechanism(s) implicated in the antagonism of IL-6/IL-17-facilitated tumor invasion of EMT6 by T-cells in DLN cells from CD200R1KO mice noted above may reflect a direct action on the tumor cells themselves, or an indirect action on a cytokine or chemokine-induced pathway, although there was no evidence from our studies that DLN cells simply acted in a cytostatic or cytostasis role. Here, IL17A is linked to neoplasm.