Recent studies have revealed important roles for the cytokine IL-17A in protective immunity against certain infections as well as roles in promoting tissue damage in hypersensitivity diseases, such as psoriasis. The aim of this PhD thesis was to investigate the regulation of IL-17A. In the first part we show that blocking PI3Kδ and PI3Kγ function impaired disease development and reduced IL-17A levels, especially from γδ T cells, in the mouse IMQ induced psoriasis-like model and impaired cytokine production in human cells from psoriasis patients. In the second part we describe the potential regulatory function of CD14+CD16- monocytes which inhibited in vitro IL-17A production from human memory CD4+ T cells and these effects were mediated by H2O2.