Introduction

Psoriasis is one of the most common and most studied inflammatory skin diseases in medicine, yet we still don’t completely understand how it develops. The disease follows a chronic, relapsing-remitting course (symptoms come and go in cycles) and manifests most commonly as raised, red, scaly patches called plaques. These plaques result from an abnormally accelerated cycle of skin cell growth: where a normal skin cell matures and sheds over the course of roughly 40–56 days, psoriatic skin cells complete this cycle in just 4–7 days. The result is a visible build-up of thick, silvery scales on the skin’s surface.

But the visible skin manifestation is only one dimension of the disease. Over the past three decades, research has firmly established psoriasis as a systemic inflammatory condition, one that affects not just the skin but the joints, cardiovascular system, metabolism, and mental health. Patients with severe psoriasis have a life expectancy approximately 3–5 years shorter than the general population, with cardiovascular disease contributing significantly to this gap (Ni & Chiu, 2014).

The modern understanding of psoriasis represents a triumph of translational immunology (turning laboratory discoveries about the immune system into real treatments). Once researchers identified the specific immune pathway driving the disease, the IL-23/Th17 axis, everything changed. New biologic therapies could now target it directly. Most patients achieve complete or near-complete skin clearance (Armstrong & Read, 2020).