Psoriasis is a chronic inflammatory skin condition affecting 2-3% of the global population, with chronic plaque psoriasis being the most prevalent form. The disease is characterized by abnormal proliferation of keratinocytes (KCs) and immune cell infiltration, leading to scaly plaques. The pathogenesis involves genetic, epigenetic, and environmental factors, with immune-mediated inflammatory responses playing a crucial role. Immune cells, including dendritic cells (DCs), CD4+ T helper cells (Th), γδ T cells, macrophages, neutrophils, and T cells, are key players in the inflammatory process. DCs bridge innate and adaptive immunity, while Th17 and Th1 cells are major pathogenic subsets. Macrophages polarize into M1 (pro-inflammatory) and M2 (anti-inflammatory) subtypes, with M1 contributing to inflammation. Neutrophils play a role in both acute and chronic inflammation, and myeloid-derived suppressor cells (MDSCs) regulate immune responses. Adaptive immune cells, such as CD4+ T cells, Th17, Th2, Th22, and Treg cells, contribute to the cytokine profile and immune feedback in psoriasis. Emerging therapies, including TNF-α inhibitors, IL-17 inhibitors, and IL-23 inhibitors, have shown significant clinical efficacy in managing psoriasis symptoms. These treatments target specific immune cells and cytokines to modulate the inflammatory response, providing new options for patients. Further research is needed to understand the complex interactions within the epithelial immune microenvironment (EIME) and develop more effective therapies.Psoriasis is a chronic inflammatory skin condition affecting 2-3% of the global population, with chronic plaque psoriasis being the most prevalent form. The disease is characterized by abnormal proliferation of keratinocytes (KCs) and immune cell infiltration, leading to scaly plaques. The pathogenesis involves genetic, epigenetic, and environmental factors, with immune-mediated inflammatory responses playing a crucial role. Immune cells, including dendritic cells (DCs), CD4+ T helper cells (Th), γδ T cells, macrophages, neutrophils, and T cells, are key players in the inflammatory process. DCs bridge innate and adaptive immunity, while Th17 and Th1 cells are major pathogenic subsets. Macrophages polarize into M1 (pro-inflammatory) and M2 (anti-inflammatory) subtypes, with M1 contributing to inflammation. Neutrophils play a role in both acute and chronic inflammation, and myeloid-derived suppressor cells (MDSCs) regulate immune responses. Adaptive immune cells, such as CD4+ T cells, Th17, Th2, Th22, and Treg cells, contribute to the cytokine profile and immune feedback in psoriasis. Emerging therapies, including TNF-α inhibitors, IL-17 inhibitors, and IL-23 inhibitors, have shown significant clinical efficacy in managing psoriasis symptoms. These treatments target specific immune cells and cytokines to modulate the inflammatory response, providing new options for patients. Further research is needed to understand the complex interactions within the epithelial immune microenvironment (EIME) and develop more effective therapies.