Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated

Dear Colleagues,

Psoriasis is a chronic inflammatory skin disease characterized by abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes. Psoriatic patients are associated with arthritis in 6%–42% of cases, and are frequently associated with cardiometabolic syndromes. The dominance of the TNF-a/IL-23/IL-17 cytokine axis plays a central role in the immunopathogenesis of psoriasis, and treatment targeting these cytokines has remarkably improved the symptoms. In psoriatic skin lesions, TNF-a produced by pathogenetic dermal dendritic cells activates the same cells in an autocrine manner, and induces them to produce IL-23, which promotes the expansion of IL-17-producing cells like Th17, gdT, or type 3 innate lymphoid cells. Several chromosomal loci and single-nucleotide polymorphisms with susceptibility to psoriasis have been identified (PSORS1 locus, IL-23R, and IL-12B genes, etc.), In genetically susceptible individuals, exposure to environmental triggers like infection or biomechanical stress initiates an inflammatory cascade, ultimately creating a sustained inflammation. Epigenetic modifications of DNA methylation or histone acetylation/methylation are associated with the development of psoriasis. In this Special Issue, we will publish updated information regarding pathogenesis, comorbidities, and therapy of psoriasis. We warmly welcome your submissions of original papers and reviews based on results at the molecular level.

Prof. Naoko Kanda
Guest Editor

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