Psoriasis is a systemic, chronic immune disease that affects the skin, nails, and joints of 3% to 4% of the US population.2 The disease is both disfiguring and disabling, causing not only physical discomfort but taking a toll on work-related activities, social relationships, and mental health, leading to poor quality of life.2

Of the approximately 7.5 million people in the United States with psoriasis, one-fifth have moderate-to-severe disease,1 in which the condition covers at least 10% of their body surface area,4 and 80% to 90% have plaque psoriasis, the most common form.1

Psoriasis is an immune-mediated inflammatory disorder believed to result from a complex interaction of environmental factors, T cells, dendritic cells, cytokines, and genetic loci. Specifically, the cytokine interleukin (IL)-17, secreted by type 1 T helper cells, is critical in development of psoriasis, while IL-12 and IL-23, pro-inflammatory cytokines, have been shown to drive type 17 T helper cell activation.

The US Food and Drug Administration (FDA) has approved six biologic agents for the treatment of moderate-to-severe plaque psoriasis. Each was developed based on an increased understanding of the pathogenesis of psoriasis. Adalimumab, etanercept, and infliximab are tumor necrosis factor-alpha (TNF-alpha) antagonists; ustekinumab is an IL-20/23p40 inhibitor; and secukinumab and ixekizumab are IL-17A inhibitors.4