Abstract
ABSTRACT: Psoriasis is a chronic immune-mediated disease, and several cytokine pathways in the psoriatic cascade have been identified and investigated as clinical targets for systemic therapy. This review provides an overview of psoriasis, including discussion of clinical variants, environmental and genetic risk factors, known comorbidities, treatment strategies, and limitations in evaluating disease severity. The manuscript then focuses on addressing how existing biologics target the various pathways described in the pathogenesis of psoriasis, how modulating these mechanisms can improve outcomes over time, and how new insights have led to the development of agents that can target different pathways associated with the disease. Overall, biologics that target tumor necrosis factor-[alpha] or interleukin-12/23 have established themselves as effective, well-tolerated treatment options for chronic plaque psoriasis that can quickly produce dramatic clinical improvement. Unlike topical, phototherapy, and conventional systemic therapies that do not specifically target the underlying pathogenesis of psoriasis, biologics have been, and continue to be, developed based on identifying therapeutic targets within the immune and inflammatory pathways associated with disease development and progression. Recently, interleukin-17A has been identified as a central cytokine driver in the pathogenesis of psoriasis, and biologic therapy targeting this cytokine has recently been approved.