In this study, we explored for the first time the levels and functional capacity of peripheral pro-inflammatory phenotypically characterized as Th17 population (CCR6+ and CCR4+), Th1 subset (CXCR3+ CCR6− and CCR4−), and sub-populations of Th17 that have switched into IFNγ producing (Th1 like cells) (CCR6+ CCR4− CXCR3+) [14–16] in psoriasis patients at baseline and at 3 months after initiation of treatment with anti-IL-17 or anti-IL-17R targeted biologic therapy. Here, IL17A is linked to psoriasis.