Psoriasis

Psoriasis is genetically determined, and the literature also describes contributions from genetic background and immune function. Review material further notes roles for epigenetic mechanisms and interaction of the skin flora in its pathophysiology. The supplied grounding does not support a single external cause.

The fundamental pathologic feature is accelerated epidermopoiesis, with hyperproliferation and disturbed differentiation of epidermal keratinocytes. Psoriasis is mediated by T cells and dendritic cells, with inflammatory myeloid dendritic cells releasing IL-23 and IL-12 to activate IL-17-producing T cells, Th1 cells, and Th22 cells. These cells produce cytokines including IL-17, IFN-γ, TNF, and IL-22, which act on keratinocytes to amplify inflammation.

The supplied grounding supports genetic susceptibility as a risk factor. It also indicates associations with systemic comorbidities such as psoriatic arthritis, cardiometabolic disease, depression, gastrointestinal disease, kidney disease, malignancy, infection, and mood disorders, but does not establish these as causal risk factors for developing psoriasis. No other specific risk factors are supported in the grounding.

For mild psoriasis, topical therapy remains the mainstay and includes topical corticosteroids, vitamin D analogues, calcineurin inhibitors, and keratolytics. Biologics are recommended as an option for first-line treatment in guidelines, and approved targeted therapies include agents that block IL-23, IL-17, or IL-17RA. The grounding also supports monoclonal antibody therapy and adalimumab as part of the biologic treatment landscape.