Human skin has long been known as a protective organ, acting as a mechanical barrier towards the external environment. More recent is the acquisition that in addition to this fundamental role, the complex architecture of the skin hosts a variety of immune and non-immune cells playing preeminent roles in immunological processes aimed at blocking infections, tumor progression and migration, and elimination of xenobiotics. On the other hand, dysregulated or excessive immunological response into the skin leads to autoimmune reactions culminating in a variety of skin pathological manifestations. Among them is psoriasis, a multifactorial, immune-mediated disease with a strong genetic basis. Psoriasis affects 2-3% of the population; it is associated with cardiovascular comorbidities, and in up to 30% of the cases, with psoriatic arthritis. The pathogenesis of psoriasis is due to the complex interplay between the genetic background of the patient, environmental factors, and both innate and adaptive responses. Moreover, an autoimmune component and the comprehension of the mechanisms linking chronic skin inflammation with systemic and joint manifestations in psoriatic patients is still a major challenge. The understanding of these mechanisms may offer a valuable chance to find targetable molecules to treat the disease and prevent its progression to severe systemic conditions.
Keywords: inflammation; memory T cell phenotype; psoriasis; psoriatic arthritis; skin immunology.