Psoriasis is a chronic inflammatory skin disease with a relapsing-remitting course, affecting over 125 million people worldwide. It is characterized by skin inflammation, keratinocyte hyperproliferation, and immune cell infiltration. The pathogenesis of psoriasis involves a complex network of immune cells and signaling pathways, including T cells, dendritic cells, neutrophils, and keratinocytes. Key players in psoriasis are T(H)17 cells, which produce pro-inflammatory cytokines such as IL-17, IFN-γ, and IL-22, and dendritic cells that promote T(H)17 differentiation through TNF-α and IL-23. Keratinocytes also contribute to inflammation by secreting chemokines and antimicrobial peptides. Other immune cells, such as T(H)9, T(H)22, and γδ T cells, also play roles in psoriasis. The dysregulation of cytokine networks, including IL-23, IL-17, and TNF-α, is central to psoriasis pathogenesis. Immune cells such as neutrophils, monocytes, and mast cells contribute to inflammation through the release of cytokines and extracellular traps. Innate lymphoid cells, including ILC3, also participate in psoriasis. T regulatory cells are impaired in psoriasis, contributing to immune dysregulation. The role of non-immune cells, such as keratinocytes, fibroblasts, and endothelial cells, is also crucial in psoriasis. Recent high-throughput studies have identified novel signaling pathways and cell populations involved in psoriasis. These findings have led to a better understanding of psoriasis pathogenesis and have influenced the development of new therapeutic strategies. Understanding the immune mechanisms in psoriasis is essential for the development of novel treatments and improved clinical management of patients.Psoriasis is a chronic inflammatory skin disease with a relapsing-remitting course, affecting over 125 million people worldwide. It is characterized by skin inflammation, keratinocyte hyperproliferation, and immune cell infiltration. The pathogenesis of psoriasis involves a complex network of immune cells and signaling pathways, including T cells, dendritic cells, neutrophils, and keratinocytes. Key players in psoriasis are T(H)17 cells, which produce pro-inflammatory cytokines such as IL-17, IFN-γ, and IL-22, and dendritic cells that promote T(H)17 differentiation through TNF-α and IL-23. Keratinocytes also contribute to inflammation by secreting chemokines and antimicrobial peptides. Other immune cells, such as T(H)9, T(H)22, and γδ T cells, also play roles in psoriasis. The dysregulation of cytokine networks, including IL-23, IL-17, and TNF-α, is central to psoriasis pathogenesis. Immune cells such as neutrophils, monocytes, and mast cells contribute to inflammation through the release of cytokines and extracellular traps. Innate lymphoid cells, including ILC3, also participate in psoriasis. T regulatory cells are impaired in psoriasis, contributing to immune dysregulation. The role of non-immune cells, such as keratinocytes, fibroblasts, and endothelial cells, is also crucial in psoriasis. Recent high-throughput studies have identified novel signaling pathways and cell populations involved in psoriasis. These findings have led to a better understanding of psoriasis pathogenesis and have influenced the development of new therapeutic strategies. Understanding the immune mechanisms in psoriasis is essential for the development of novel treatments and improved clinical management of patients.