Monoclonal antibodies inhibiting IL-12, -23, and -17 for the treatment of psoriasis

Abstract

Psoriasis is a chronic, inflammatory, immune-mediated skin condition that affects 3 to 4% of the adult US population, characterized by well-demarcated, erythematous plaques with silver scale. Psoriasis is associated with many comorbidities including cardiometabolic disease and can have a negative impact on quality of life. The current armamentarium of psoriasis treatment includes topical therapies, phototherapy, oral immunosuppressive therapies, and biologic agents. Over the past 2 decades, there has been rapid development of novel biologic therapies for the treatment of moderate-to-severe plaque psoriasis. This article will review the role of IL-12, IL-23, and IL-17 in the pathogenesis of psoriasis and the monoclonal antibodies (ustekinumab, secukinumab, ixekizumab, brodalumab, guselkumab, tildrakizumab, and risankizumab) that target these cytokines in the treatment of this disease.

Figure 1.

The pathogenesis of psoriasis. Abbreviations: DDC – dermal dendritic cells, AMP – anti-microbial peptides, IL – interleukin, Th1 – T-helper type 1, Th17 – T-helper type 17, Th22 – T-helper type 22, TNF-α – tumor necrosis factor – α, INF-γ – interferon-gamma.