Interleukin-17 and Interleukin-23: A Narrative Review of Mechanisms of Action in Psoriasis and Associated Comorbidities

Psoriasis is an immune-mediated inflammatory skin disease associated with numerous inflammatory comorbidities, including increased cardiovascular risk. The interleukin (IL)-23/IL-17 axis plays a central role in the immunopathogenesis of psoriasis and related comorbidities by acting to stimulate keratinocyte hyperproliferation and feed-forwarding circuits of perpetual T cell-mediated inflammation. IL-17 plays an important role in the downstream portion of the psoriatic inflammatory cascade. This review discusses the distinct mechanisms of action of IL-17 and IL-23 in the immunopathogenesis of psoriasis and related comorbidities plus the significant therapeutic benefits of selectively inhibiting these cytokines in patients with moderate to severe plaque psoriasis.

Automated summary

Psoriasis is an immune-mediated inflammatory skin disease associated with inflammatory comorbidities, including increased cardiovascular risk. The IL-23/IL-17 axis plays a central role in the immunopathogenesis of psoriasis and related comorbidities, and selectively inhibiting these cytokines has significant therapeutic benefits for patients with moderate to severe plaque psoriasis.