There is currently a translational revolution in the treatment and management of psoriasis, according to a recent review, and emerging bispecific antibodies offer the potential for even better disease control, whereas small-molecule drugs offer future alternatives to the use of biologics and less costly long-term disease management. During the last 2 decades, the discovery of the central role for the IL-23/type 17 T-cell axis in the development of psoriasis has led to a major paradigm shift in the pathogenic model for this condition. The activation and upregulation of IL-17 in pre-psoriatic skin produces a “feed forward” inflammatory response in keratinocytes that is self-amplifying and drives the development of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and recruitment of leukocyte subsets into the skin. Clinical trial data for monoclonal antibodies against IL-17 signaling, such as secukinumab, and newer IL-23p19 antagonists underscore the central role of these cytokines as predominant drivers of psoriatic disease.
Hawkes JE, Chan TC, Krueger JG. Psoriasis pathogenesis and the development of novel targeted immune therapies. J Allergy Clin Immunol. 2017;140(3):645-653. doi:10.1016/j.jaci.2017.07.004.
The introduction of IL-17 and IL-23 antagonists for the treatment of psoriatic disease has resulted in changes in the primary endpoints being used in clinical trials. Due to the high efficacy and rapid clearance with IL-17 and IL-23 antagonists, PASI 90 and PASI 100 responses are now considered better targets than the PASI 75 response. The IL-17 inhibitors, including the FDA-approved secukinumab, and the IL-23 p19 antagonists do underscore the central role of these cytokines as predominant drivers of psoriatic disease. —Paul S. Yamauchi, MD, PhD
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