Psoriasis: Treatment and Pathogenesis

Psoriasis is a chronic inflammatory skin disease driven by a dysregulated immune response in which a subset of T cells, known as TH17 cells, produce interleukin-17 and other inflammatory cytokines that trigger rapid, abnormal proliferation of skin cells. Central to understanding why this response spirals out of control is the relationship between TH17 cells and regulatory T cells, two lineages that arise from shared precursors but are pushed in opposing directions by cytokines like TGF-β and interleukin-23. Researchers are working to clarify how the balance between these populations breaks down in psoriatic skin, and why interleukin-23 appears to sustain pathogenic inflammation even after initial triggers resolve. A key open question is whether restoring regulatory T cell function, rather than simply blocking individual cytokines, could offer more durable disease control.

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Keywords

IL-17TH17 CellsInterleukin-23Autoimmune InflammationPsoriasisTGF-ß