Pathogenesis of psoriasis: past, present, future

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Psoriasis is a common, chronic, systemic immune-mediated inflammatory disease that affects the skin, joints, and other organs and systems. Despite the fact that psoriasis is one of the most studied dermatoses, its pathogenesis has not yet been fully clarified. In recent years, the pathogenetic model leading to the formation of psoriatic papules and plaques has undergone significant changes.
 This article presents a retrospective analysis of the study of the disease over the past 60 years from the generally accepted concept of epidermal dermatosis to understanding the complex interactions between keratinocytes, dendritic cells, T-lymphocytes, neutrophils and mast cells, with a significant role of interleukins (IL) 23, 17, 22,10, T-helper cells (Th) 17, 22, T-regulatory cells, transformative growth factor b1 (TGF-b1), in the pathogenesis of the disease. Targeted therapy using new biologics and small molecules, patient education, screening for comorbidities, and regular patient follow-up allow to apply a personalized approach to the patient and achieve impressive results.
 Achievements in psoriasis research have led to the fact that today we are witnessing the so-called translational revolution in psoriasis therapy, consisting in the fastest possible transfer of fundamental discoveries of the field of theoretical research to the field of practical application.