Psoriasis is a chronic immune-mediated inflammatory dermatosis driven by the IL-23/IL-17 axis. In genetically susceptible individuals (HLA-Cw6 is the strongest genetic association), environmental triggers (trauma/Koebner phenomenon, infections such as streptococcal pharyngitis, stress, medications including lithium, beta-blockers, antimalarials, and abrupt corticosteroid withdrawal) activate dendritic cells that migrate to skin-draining lymph nodes and release IL-12 and IL-23. IL-23 drives differentiation and expansion of Th17 cells, which produce IL-17A, IL-17F, and IL-22. These cytokines act on keratinocytes to induce hyperproliferation (epidermal turnover accelerated from ~28 days to 3-5 days), impaired differentiation (resulting in parakeratosis and retention of nuclei in the stratum corneum), and production of antimicrobial peptides and chemokines that amplify the inflammatory cycle. The result is well-demarcated erythematous plaques with silvery-white micaceous scale. Biologic therapies target specific nodes in this pathway: TNF-alpha inhibitors (adalimumab, etanercept), IL-12/23 inhibitors (ustekinumab), IL-23p19 inhibitors (guselkumab, risankizumab), IL-17A inhibitors (secukinumab, ixekizumab), and IL-17 receptor A blockers (brodalumab). JAK inhibitors (tofacitinib, deucravacitinib/TYK2 inhibitor) target intracellular signaling downstream of multiple cytokine receptors.