Psoriasis is a chronic inflammatory skin disease characterized by chronic, relapsing-remitting symptoms. Recent research has revealed a complex network of interactions between immune cells and other cell types in its pathogenesis. Dendritic cells, T<Hsub>17</Hsub> cells, and keratinocytes form a pathogenic triad, with dendritic cells producing TNF-α and IL-23 to promote T<Hsub>17</Hsub> cell differentiation, which then produce key cytokines such as IL-17, IFN-γ, and IL-22. These cytokines lead to skin inflammation and hyperproliferation of keratinocytes. Other cell types and signaling pathways, including T<Hsub>9</Hsub> cells, T<Hsub>22</Hsub> cells, CD8⁺ cytotoxic cells, neutrophils, γδ T cells, and cytokines and chemokines secreted by them, also play significant roles in psoriasis pathogenesis. High-throughput analysis of lesional skin has identified novel signaling pathways and cell populations involved in the disease. Understanding the immune response in psoriatic inflammation is crucial for developing new therapeutic strategies and improving clinical management. The review comprehensively presents the dysregulation of immune response in psoriasis, emphasizing recent findings on the roles of various immune cells and non-immune cells.Psoriasis is a chronic inflammatory skin disease characterized by chronic, relapsing-remitting symptoms. Recent research has revealed a complex network of interactions between immune cells and other cell types in its pathogenesis. Dendritic cells, T<Hsub>17</Hsub> cells, and keratinocytes form a pathogenic triad, with dendritic cells producing TNF-α and IL-23 to promote T<Hsub>17</Hsub> cell differentiation, which then produce key cytokines such as IL-17, IFN-γ, and IL-22. These cytokines lead to skin inflammation and hyperproliferation of keratinocytes. Other cell types and signaling pathways, including T<Hsub>9</Hsub> cells, T<Hsub>22</Hsub> cells, CD8⁺ cytotoxic cells, neutrophils, γδ T cells, and cytokines and chemokines secreted by them, also play significant roles in psoriasis pathogenesis. High-throughput analysis of lesional skin has identified novel signaling pathways and cell populations involved in the disease. Understanding the immune response in psoriatic inflammation is crucial for developing new therapeutic strategies and improving clinical management. The review comprehensively presents the dysregulation of immune response in psoriasis, emphasizing recent findings on the roles of various immune cells and non-immune cells.