The epidermal immune microenvironment plays a central role in the pathogenesis of psoriasis.

Psoriasis is a chronic immune-mediated skin disease whose inflammation can affect other systems and lead to various comorbidities. As a model inflammatory skin disease, while advances in mechanistic insights and targeted therapies have improved outcomes, unmet clinical needs persist. Modern technologies like single-cell sequencing and spatial transcriptomics reveal that skin immunity operates as a complex network involving neuroregulation, symbiotic microbial immunity, metabolic abnormalities, and reprogramming. These findings underscore the complexity of the local immune microenvironment in the skin and its central role in disease pathogenesis. In psoriatic inflammation, the epidermal immune microenvironment - driven by keratinocytes, dendritic cells, T cells, and skin microbiota - emerges as a core pathogenic mechanism. Keratinocytes, acting as both inflammatory effectors and disease drivers, interact with immune cells to initiate and amplify responses. Studying this microenvironment offers novel therapeutic targets for psoriasis and related inflammatory skin diseases.