Psoriasis

Plaque psoriasis is a chronic immune-mediated inflammatory disease, not merely an accelerated process of skin shedding. Dendritic-cell production of IL-23 sustains pathogenic Th17 cells, which release IL-17A, IL-17F, and TNF-alpha. These signals drive keratinocyte proliferation, abnormal differentiation, chemokine release, and neutrophil recruitment. The epidermis therefore thickens and sheds incompletely, producing the familiar sharply bordered plaque with adherent silvery scale. The same mechanism explains why advanced therapies can be selective. TNF inhibitors, IL-17-directed agents, and IL-23-directed agents interrupt different points in the inflammatory circuit rather than suppressing immunity indiscriminately. A therapy that works well for plaque psoriasis should not automatically be assumed to treat every psoriasis phenotype. Generalized pustular psoriasis (GPP) has a different dominant pathway. Dysregulated IL-36 signalling promotes a sudden, widespread neutrophilic pustular eruption, often with fever and systemic illness. This distinction has practical consequences: an IL-36 receptor antagonist, spesolimab, is specifically used for GPP flares, whereas IL-17 or IL-23 treatment is not a substitute for that targeted approach during an acute flare. Trauma, infection, psychological stress, and some medications can precipitate or worsen disease in susceptible people. New...