Keratinocyte Med1 shapes an epidermal-dermal-immune axis in a mouse model of psoriasis-like dermatitis

Our results showed that keratinocyte-specific deletion of Med1 markedly attenuated imiquimod-induced psoriasiform inflammation, suppressed keratinocyte inflammatory gene programs and normalized differentiation dynamics. Single-cell transcriptomic analyses revealed that Med1 deficiency selectively impeded IL-17–responsive programs in reticular fibroblasts and reduced the recruitment and effector functions of pathogenic IL-17–producing γδ T cells. Single-cell ATAC‑seq demonstrated that Med1 selectively increased chromatin accessibility at promoter loci of psoriasis‑associated genes in keratinocytes, thereby precisely amplifying inflammatory feedback loops. Bulk RNA-seq data were collected from mouse epidermis (CON and IMQ); scRNA-seq data were collected from IMQ-induced mouse psoriasiform whole skin; scATAC-seq data were collected from IMQ-induced mouse psoriasiform epidermis.