Although the exact mechanism responsible for the pathogenesis of psoriasis is unclear, interferon-γ producing type 1 T cells have been reported to play a significant role. Infiltrating activated type 1 T cells in the lesions are believed to be responsible for stimulating keratinocytes, which produce many cytokines and growth factors. The hyperproliferative epidermis is understood to be the result of either the cytokines produced by the intraepidermal T cells or the reactive phenomenon after keratinocyte damage. The microenvironment in psoriatic lesions deviates toward the type 1 status, because of the increased type 1 cytokines and either the decreased or unchanged type 2 cytokines observed in psoriatic lesions. Therefore, this review focused on a T-cell-mediated immunological basis for the current hypothesis of the psoriasis pathogenesis.