Vol. 6, Issue 2, Part A (2024)

Psoriasis is a chronic, immune-mediated inflammatory skin disorder that significantly affects patients' quality of life. It is characterized by the hyperproliferation of keratinocytes and a dysregulated immune response, with systemic inflammation playing a central role in disease progression. Tumor necrosis factor-alpha (TNF-α) and interleukin-17 (IL-17) are two crucial cytokines that drive the inflammatory pathways in psoriasis, making them prime targets for therapeutic intervention. The development of biologic agents that selectively inhibit TNF-α and IL-17 has transformed the treatment landscape, providing new hope for patients with moderate to severe forms of the disease. These biologics offer a significant advantage over conventional therapies, demonstrating superior efficacy, faster onset of action, and a better safety profile in clinical trials. This paper presents a comprehensive review of the pathophysiological roles of TNF-α and IL-17 in psoriasis and the mechanisms by which biologic agents targeting these cytokines mitigate disease symptoms. Furthermore, it discusses the clinical efficacy of these agents, focusing on pivotal trials that have established their place in psoriasis management. The review also examines long-term outcomes and the potential for sustained disease remission, as well as safety concerns, including the risk of infections and adverse effects associated with these therapies. In addition, the paper explores future directions for biologic treatments in psoriasis, including emerging therapies and strategies for optimizing long-term disease control. Through this review, we aim to provide insight into the evolving therapeutic approaches for psoriasis and their impact on patient outcomes.