The pathogenic model of psoriasis has recently changed to focus on the induction of disease by a central cytokine pathway in which over-expression of IL-23 in psoriasis lesions drives expansion and activation of T-cells that over-produce IL-17. T-cells that produce IL-17 in psoriasis lesions are mainly conventional CD4+ and CD8+ T-cells that are designated as Th17 and Tc17, respectively. However, less abundant subsets such as γδ T-cells or innate lymphoid cells may also contriubute to IL-17 production in psoriasis lesions, so the entire set of IL-17 producing lymphocytes is now called Type 17 (T17) cells. IL-17 acts as pathogenic cytokine in psoriasis principally through inducing transcription of many other cytokines and inflammatory mediators in keratinocytes. Some of the induced products, e.g., S100A7 are molecules typify psoriasis, while others create “feed-forward” inflammatory circuits that regulate epidermal hyperplasia, influx of many different leukocyte types, and control expression of newly discovered psoriasis auto-antigens. Thus psoriasis becomes a self-perpetuating inflammatory reaction in focal skin areas due to chronic T-cell activation by autoantigens that are produced at high levels in skin lesions. This chronic immune process can be significantly reduced or eliminated through therapeutic targeting of either IL-23 or IL-17A with monoclonal antibodies. Targeting psoriasis with IL-17A monoclonal antibodies (secukinumab or ixekizumab) leads not only to impressive clinical improvement in the majority of treated patients, but it largely reverses epidermal changes that are IL-17 induced and it dramatically reduces immune cell infiltrates and molecular changes that are associated with psoriasis. Systemic inflammation, as measured by over production of IL-17 induced genes in leukocytes can be rapidly attenuated by IL-17 antibodies, but maximal benefit to the disease phenotype occurs only with long-term treatment, e.g., recent study show more disease improvement after 1 year of secukinumab treatment, compared to results obtained from 12-16 weeks of treatment.