The important role of CD8+ T-cells in the pathogenesis of psoriasis is well-determined. However, besides type 1 cytokines that were formerly known, it was recently found that these cells secrete type 17 and type 22 cytokines. The majority of IL-17A+CD8+ T-cells in the blood belong to a subset of innate T-cells named mucosa-associated invariant T-cells (MAIT). However, the majority of IL-17A+CD8+ T-cells in psoriatic epidermis are conventional T-cells and are up-regulated in psoriasis. In contrast to Th17 cells that secrete only IL-17, Tc17 cells secrete IFN-ϒ, TNF-α, CCL20, IL-22, and granzyme B as well. The key cytokine is IL-17A, which promotes keratinocyte hyperproliferation and stimulates them to produce other proinflammatory cytokines. These activities initiate and propagate the inflammation and architectural changes in the skin that clinically manifest as psoriatic lesions. However, a relatively novel cell subtype named Tc22 has been discovered in psoriasis that could secrete IL-22 in the absence of IL-17 and IFN-gamma. IL-22 stimulates proliferation and de-differentiation of keratinocytes, subsequently leading to epidermal acanthosis. As the understanding of the pathogenesis of psoriasis increases, the new selective therapies may offer an optimal balance between increased clinical benefit and reduced risk of side-effects.