Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Abstract

Mechanical scratching, a common external stress affecting the skin, is induced by various causes, such as pruritus. Scratch injury to epidermal keratinocytes upregulates the production and release of chemokine (C‐C motif) ligand 20 (CCL20) in vitro , which selectively chemoattracts interleukin (IL)‐17A‐producing immune cells that express chemokine (C‐C motif) receptor 6 (CCR6). In IL‐17A‐dominant psoriasis, scratch‐induced CCL20 upregulation and subsequent accumulation of IL‐17A‐producing immune cells and CCR6⁺ mature dendritic cells may trigger the development of psoriatic lesions, a process known as the Koebner phenomenon. In IL‐4/IL‐13‐dominant atopic dermatitis, pruritus and subsequent scratching are the primary symptoms. Scratch‐induced CCL20 production from keratinocytes may explain why IL‐17A levels are also elevated in atopic dermatitis. In contrast, mechanical scratching is likely to negatively regulate IL‐13 signaling by upregulating the expression of IL‐13 receptor α2, which serves as a decoy receptor for IL‐13 in keratinocytes. In this review, we summarize current reports on topics related to the pathogenic role of epidermal scratch injury in psoriasis and atopic dermatitis.