Psoriasis is a chronic inflammatory skin disease with a strong genetic component and autoimmune features. It affects about 2% of the global population, with higher prevalence in Caucasian and Scandinavian populations. The disease has various clinical subtypes, including plaque psoriasis (the most common), inverse psoriasis, guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. Psoriasis is associated with comorbidities such as metabolic syndrome, cardiovascular disease, and psoriatic arthritis. It significantly impacts quality of life, comparable to cancer and depression. The pathogenesis of psoriasis involves sustained inflammation leading to uncontrolled keratinocyte proliferation and dysfunction. Key inflammatory pathways include the IL-23/Th17 axis and TNF-α signaling. Psoriasis is driven by immune cells such as dendritic cells, T cells, and macrophages, and involves the production of cytokines like IL-17, IL-23, and TNF-α. Genetic factors, including HLA-Cw6, play a significant role in psoriasis susceptibility. Epigenetic modifications, such as DNA methylation and miRNA expression, also contribute to the disease. Psoriasis therapy includes small-molecule drugs like methotrexate, cyclosporine, and apremilast, as well as biologics targeting specific pathways. Biologics such as TNF-α inhibitors (etanercept, infliximab, adalimumab, certolizumab) and IL-23/Th17 inhibitors (ustekinumab, guselkumab, tildrakizumab, risankizumab, secukinumab, ixekizumab, brodalumab) are effective in treating psoriasis. These therapies have shown significant improvements in disease severity and patient outcomes. The choice of treatment depends on disease severity, comorbidities, and patient factors. Psoriasis management requires long-term strategies to control symptoms and reduce the burden of disease.Psoriasis is a chronic inflammatory skin disease with a strong genetic component and autoimmune features. It affects about 2% of the global population, with higher prevalence in Caucasian and Scandinavian populations. The disease has various clinical subtypes, including plaque psoriasis (the most common), inverse psoriasis, guttate psoriasis, pustular psoriasis, and erythrodermic psoriasis. Psoriasis is associated with comorbidities such as metabolic syndrome, cardiovascular disease, and psoriatic arthritis. It significantly impacts quality of life, comparable to cancer and depression. The pathogenesis of psoriasis involves sustained inflammation leading to uncontrolled keratinocyte proliferation and dysfunction. Key inflammatory pathways include the IL-23/Th17 axis and TNF-α signaling. Psoriasis is driven by immune cells such as dendritic cells, T cells, and macrophages, and involves the production of cytokines like IL-17, IL-23, and TNF-α. Genetic factors, including HLA-Cw6, play a significant role in psoriasis susceptibility. Epigenetic modifications, such as DNA methylation and miRNA expression, also contribute to the disease. Psoriasis therapy includes small-molecule drugs like methotrexate, cyclosporine, and apremilast, as well as biologics targeting specific pathways. Biologics such as TNF-α inhibitors (etanercept, infliximab, adalimumab, certolizumab) and IL-23/Th17 inhibitors (ustekinumab, guselkumab, tildrakizumab, risankizumab, secukinumab, ixekizumab, brodalumab) are effective in treating psoriasis. These therapies have shown significant improvements in disease severity and patient outcomes. The choice of treatment depends on disease severity, comorbidities, and patient factors. Psoriasis management requires long-term strategies to control symptoms and reduce the burden of disease.