We hypothesized that while IL-6/IL-17 were primary mediators of tumor invasion for both 4THM and EMT6 tumor cells, an independent function of the added DLN cells could lead to the attenuation of EMT6 tumor invasion, and the data implicated a role for non T depleted (but not T depleted) DLN cells from CD200RKO mice in this function. The gene discussed is IL17A; the disease is neoplasm.