Unveiling the IL-17 axis: an immunometabolic bridge between psoriasis and metabolic syndrome

Psoriasis is increasingly recognized as a systemic inflammatory disease frequently associated with a cluster of cardiometabolic comorbidities, including obesity, type 2 diabetes, and cardiovascular disease. Central to this association is the interleukin-17 (IL-17) signaling axis, a key driver of both cutaneous inflammation and systemic metabolic dysfunction.

This review examines the complex immunometabolic interactions mediated by IL-17 and synergistic cytokines such as TNF‑α, IL‑6, IL‑1β, IL‑23, and adipokines, which contribute to endothelial dysfunction, insulin resistance, and adipose-tissue inflammation.

Beyond its established role in psoriasis pathogenesis, the IL-17 pathway is implicated in the 'psoriatic march,' linking chronic skin inflammation to accelerated atherosclerosis. The advent of IL-17 inhibitors has transformed the management of moderate-to-severe psoriasis, achieving unprecedented skin clearance (PASI 90/100). Emerging evidence suggests that these agents may also exert potential beneficial effects on selected inflammatory and cardiometabolic markers. However, their direct impact on metabolic parameters remains under investigation.

Understanding these shared molecular pathways is essential for adopting a holistic therapeutic approach that addresses both cutaneous disease and the systemic burden of psoriatic patients.