Psoriasis: Treatment and Pathogenesis

Psoriasis is a chronic inflammatory skin disease driven by a miscalibrated immune response in which T helper 17 cells and the cytokines they produce—particularly IL-17 and IL-23—sustain a self-reinforcing cycle of tissue damage. Researchers study how the same molecular signals, especially TGF-β, can tip a developing T cell toward either a destructive TH17 fate or a regulatory T cell identity that normally keeps inflammation in check, a balance that breaks down in autoimmune conditions like psoriasis. Targeted biologics blocking IL-17 or IL-23 have transformed treatment over the past decade, yet questions remain about why some patients relapse after stopping therapy and how early immune checkpoints might be corrected rather than simply suppressed. Current work is probing the precise cytokine environments that determine TH17 versus regulatory T cell commitment, with the hope of identifying interventions that restore immune tolerance rather than broadly dampen host defenses.

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Keywords

IL-17TH17 CellsInterleukin-23Autoimmune InflammationPsoriasisTGF-ß