Since the publication of the 2009 Canadian Guidelines for the Management of Plaque Psoriasis, significant advances have been made in determining the role of T cells in inflammatory and autoimmune diseases. We now understand that Th1, Th17, Treg, and Th22 cells interact with each other. Whereas psoriasis was previously thought to be a Th1-mediated disease, Th17 cells are now seen to play a pivotal role.1 Interleukin (IL)-17-producing dermal γδT cells probably play a vital role in pathogenesis. It has been proposed that psoriasis is first triggered by foreign antigens that activate dendritic cells and macrophages. The activated, professional antigen-presenting cells release IL-23 and IL-1β along with other proinflammatory cytokines. Proinflammatory cytokines in turn activate dermal γδT cells as well as other IL-17-producing cells. The host of activated cells copiously produce IL-17, which further promotes the immune response. IL-17 (primarily), IL-22, and tumor necrosis factor α (TNF-α) then induce a keratinocyte hyperproliferation. A hyperproliferative response leads to the release of chemokines. Released chemokines attract more immune effector cells into the skin. Immune effector cells (ie, neutrophils, mast cells, natural killer cells, and natural killer T cells) contribute to the proinflammatory response, resulting in escalated production of cytokines and chemokines.