Interleukin (IL)-17 and IL-23 are involved in the immunopathogenesis of psoriasis (PsO) and related comorbidities by acting to stimulate keratinocyte hyperproliferation and feed-forwarding circuits of perpetual T cell-mediated inflammation.

IL-17 and IL-23 have unique mechanisms of action in the immunopathogenesis of PsO.

Additionally, elevated levels of IL-17 and IL-23 in patients with moderate to severe PsO promote chronic subclinical inflammation that increases the risk of comorbidities.

Both IL-17 and IL-23 are implicated in PsA pathogenesis; however, IL-17-mediated inflammation may be more central in the development of cardiometabolic comorbidities and axial spondyloarthritis, whereas IL-23 may be more important in IBD immunopathogenesis.

Given the specificity of the IL-23/IL-17A axis in modulating the differentiation and activation of specialized cells involved in skin and joint inflammation, selective blockade of IL-23 and IL-17A is more efficacious than traditional biologic therapies in targeting the psoriatic disease process.