Psoriasis articles from across Nature Portfolio

Analysis of the somatic mutations landscape of 111 patients with psoriasis vulgaris shows that the disease is unlikely to be driven by clonal expansions caused by somatic mutations in keratinocytes. A mutational footprint associated with psoralen treatment was observed and characterized.

A study in Immunity reports that a high-fat diet in mice leads to the loss of PPARγ⁺ T_reg cells in the skin, which exacerbates psoriasis mediated by IL-17-producing γδ T cells.

A new study uncovers a protective role for epidermal S100A9 in psoriasis and psoriatic arthritis, and highlights this alarmin as a potential biomarker of disease progression.

The results of several retrospective studies have reported that systemic treatment in patients with psoriasis reduces the risk of incident psoriatic arthritis (PsA). Although encouraging from a prevention perspective, such studies are limited in their ability to provide a conclusive understanding of PsA risk, preventing a clear picture from emerging.

A crucial role for glucose metabolism has been identified in wound repair and in the pathogenesis of chronic inflammatory skin diseases, indicating that targeting metabolism is an approach for treating psoriasis.

The metabolite itaconate induces electrophilic stress that induces an antioxidant response and regulates secondary TLR transcriptional responses and IL-17-driven pathology.

The immunomodulatory drug dimethyl fumarate blocks GAPDH and aerobic glycolysis in activated immune cells.