RIPK1 downregulation in keratinocyte enhances TRAIL signaling in psoriasis

Psoriasis, a common inflammatory skin disorder characterized by scaly erythemas and plaques, affects around 2% of the population [1]. Dysregulated interactions of innate and adaptive immunities are deeply involved in the pathomechanism. Complexes of epidermis-derived antimicrobial peptide, LL-37, and host DNA are thought to act as an initiating factor via stimulating IFN-α-production from dermal plasmacytoid dendritic cells [2]. Consequently, activated myeloid dendritic cell (DC) populations release TNF-α and IL-23, and stimulate Th1 cells and T helper cell 17 (Th17) to produce IFN-γ, IL-17 and IL-22 [3,4].

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