Thus, in both AD and psoriasis models, Vγ2+ Tγδ17 cells are the critical mediators of skin homeostasis and acute inflammation, and the Vγ4+ counterpart, and other innate IL-17 producing T cells such as DN MAITs that are present in the dermis of Sox13-/- mice, cannot functionally compensate for the loss of Vγ2+ Tγδ17 cells. This evidence concerns the gene SOX13 and Alzheimer disease.