Psoriasis is a highly visible, chronic, immune-mediated inflammatory skin disorder that affects 2–3% of the US population (Lowes et al., 2014). Tumor necrosis factor-α (TNF-α) and IL-17A synergistically up-regulate the production of other cytokines, chemokines, and antimicrobial peptides from keratinocytes and regional immune cells, initiating and perpetuating the immune activation of psoriasis (Chiricozzi et al., 2011; Di Cesare et al., 2009; Ettehadi et al., 1994; Harden et al., 2015; Lowes et al., 2005).
