Psoriasis is a chronic autoimmune inflammatory disease characterized by abnormal keratinocyte metabolism. The development of psoriasis is closely related to immune system dysfunction, leading to the activation of inflammatory pathways in the epithelial immune microenvironment (EIME), which contributes to the development of autoimmune and inflammatory skin diseases. This review discusses the pathogenesis of psoriasis, focusing on the interactions between immune cell activation and cytokine production. It also explores the role of EIME in psoriasis and potential novel therapeutic targets. The review emphasizes the importance of immune cells in the EIME and provides insights into the mechanisms underlying psoriasis and potential therapeutic avenues. Psoriasis is influenced by genetic, epigenetic, and environmental factors. Environmental factors such as stress, infections, and sun exposure can exacerbate the condition. Epigenetic modifications play a significant role in psoriasis development. The pathogenesis of psoriasis involves the interaction of immune cells and cytokines, with TNF-α and IL-17/IL-23 playing key roles. Th17 and Th1 cells contribute to the inflammatory response, leading to keratinocyte hyperproliferation and skin lesions. Other cytokines, including IL-6, IL-36, IL-12, and IL-22, are also involved in psoriasis pathogenesis. The EIME is a crucial component of the skin's immune response, consisting of immune cells, cytokines, and sensory nerve endings. It plays a significant role in the development of psoriasis, with immune cells such as DCs, macrophages, neutrophils, and T cells contributing to the inflammatory process. Innate immune cells like DCs and macrophages, as well as adaptive immune cells like Th1, Th17, Th2, and Treg cells, are involved in psoriasis pathogenesis. The interactions between these immune cells and cytokines drive the chronic inflammatory state of psoriasis. Emerging therapies targeting immune cells in psoriasis include biologics that target specific cytokines and immune cells, as well as small molecule drugs. These therapies aim to modulate the EIME and reduce inflammation. The review highlights the importance of understanding the complex interactions between immune cells and cytokines in psoriasis to develop effective treatments. The role of immune cells in the EIME is crucial for understanding the pathogenesis of psoriasis and developing targeted therapies.Psoriasis is a chronic autoimmune inflammatory disease characterized by abnormal keratinocyte metabolism. The development of psoriasis is closely related to immune system dysfunction, leading to the activation of inflammatory pathways in the epithelial immune microenvironment (EIME), which contributes to the development of autoimmune and inflammatory skin diseases. This review discusses the pathogenesis of psoriasis, focusing on the interactions between immune cell activation and cytokine production. It also explores the role of EIME in psoriasis and potential novel therapeutic targets. The review emphasizes the importance of immune cells in the EIME and provides insights into the mechanisms underlying psoriasis and potential therapeutic avenues. Psoriasis is influenced by genetic, epigenetic, and environmental factors. Environmental factors such as stress, infections, and sun exposure can exacerbate the condition. Epigenetic modifications play a significant role in psoriasis development. The pathogenesis of psoriasis involves the interaction of immune cells and cytokines, with TNF-α and IL-17/IL-23 playing key roles. Th17 and Th1 cells contribute to the inflammatory response, leading to keratinocyte hyperproliferation and skin lesions. Other cytokines, including IL-6, IL-36, IL-12, and IL-22, are also involved in psoriasis pathogenesis. The EIME is a crucial component of the skin's immune response, consisting of immune cells, cytokines, and sensory nerve endings. It plays a significant role in the development of psoriasis, with immune cells such as DCs, macrophages, neutrophils, and T cells contributing to the inflammatory process. Innate immune cells like DCs and macrophages, as well as adaptive immune cells like Th1, Th17, Th2, and Treg cells, are involved in psoriasis pathogenesis. The interactions between these immune cells and cytokines drive the chronic inflammatory state of psoriasis. Emerging therapies targeting immune cells in psoriasis include biologics that target specific cytokines and immune cells, as well as small molecule drugs. These therapies aim to modulate the EIME and reduce inflammation. The review highlights the importance of understanding the complex interactions between immune cells and cytokines in psoriasis to develop effective treatments. The role of immune cells in the EIME is crucial for understanding the pathogenesis of psoriasis and developing targeted therapies.