Biologics for psoriasis: What is new?

Etiology of psoriasis is unclear but environmental, genetic, and immune factors act significant roles in the pathogenesis of this disease. Helper T cells (TH), plasmoid, and dermal dendritic cells play a prominent role in the development of classical psoriatic lesions. Interleukin stimulation is another important process in the pathogenesis of the disease that directly influences keratinocytes and leading to the formation of psoriatic pattern in the skin. Tumor necrosis factor (TNF) α which releases from keratinocytes activates dendritic cells in the early stages of complex pathogenesis of psoriasis. Activated keratinocytes also produce other proinflammatory cytokines (IL-1b and IL-6), antimicrobial peptides, and various chemokines. TNF activates dendritic cells that produce IL-23, leading to TH17 differentiation. TH17 cells secrete IL-17A, which has been shown to promote psoriatic skin changes. Consequently, after clarification of these main pathological mechanisms, anti-IL therapies have been accepted as a major treatment for patients with moderate-to-severe psoriasis. Here, actual information will be presented about biological agents currently in clinical use or being tested for clinical application for treatment of patients with psoriasis.