A chronic, immune-mediated inflammatory disease that affects the epidermis and has systemic implications is psoriasis. Psoriasis affects approximately 2–3% of the global population and is distinguished by immune dysregulation and hyperproliferation of keratinocytes. Recent developments in our comprehension of its pathogenesis have revealed the critical roles of genetic predisposition, environmental stimuli, and dysregulated immune pathways, particularly the interaction between Th17 cells and the IL-23/IL-17 axis. These discoveries have not only improved diagnostic accuracy but have also transformed therapeutic strategies. Traditional treatments, such as topical agents, phototherapy, and systemic therapies like methotrexate and cyclosporine, have offered symptomatic relief; however, their long-term efficacy and safety are restricted. The emergence of biologics that target the TNF-α, IL-17, and IL-23 pathways has resulted in a paradigm shift in the management of psoriasis, providing enhanced outcomes and safer alternatives. In addition, the emergence of small-molecule therapies, including PDE4 and JAK inhibitors, has expanded treatment options, particularly for patients who are intolerant or unresponsive to biologic medication. Treatment resistance, unmet requirements in paediatric and severe psoriasis cases, and the psychosocial burden of the disease persist, despite these advancements. Furthermore, the need for comprehensive, multidisciplinary therapy is underscored by the systemic characteristics of psoriasis, which is linked to comorbidities like cardiovascular disease, metabolic syndrome, and mental health issues. This review delineates the findings on psoriasis pathogenesis, diagnostic breakthroughs, and treatment improvements, highlighting the shift towards personalised therapy and pinpointing opportunities for future study.