Abstract
Substantial developments over the last decade have advanced our knowledge and understanding of psoriasis, from both a basic scientific and clinical perspective. Identification of immunopathological mechanisms involved in disease development and the elucidation of cellular processes have been, and continue to be, integral in the development of novel therapies and therapeutic approaches. Significant progress has been made in highlighting key biological pathways, some of which are shared with other autoimmune diseases. Evidence suggests a relationship between psoriasis and specific comorbidities, some with a confirmed biological basis and others, such as obesity, with intriguing but complex links to psoriasis. A new class of biologic agents selectively targeting interleukin (IL)-23p19 have shown additional efficacy in improving disease severity, even compared with those targeting both IL-12 and IL-23, highlighting the significance of IL-23 in psoriasis.1 The true relationships between comorbid conditions in patients with psoriasis and determination of the mechanisms involved will be important in the long-term management of the condition.
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