IL17A and neoplasm: Importantly, the requirement for γδ T cells in pathogenesis in this model was not evident if the mice were allowed to recover for 6 weeks after γδ T-cell depletion; this is because the niches depleted of γδ T cells were repopulated by innate lymphoid cells (ILCs) and IL-17–producing αβ lineage T cells, which were capable of compensating for the loss of γδ T cells and promoting skin inflammation72.