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"Epidermal inflammation mediators" collectively refers to a diverse group of signaling molecules—including cytokines, chemokines, antimicrobial peptides, and vasoactive compounds—that are produced by keratinocytes, skin-resident immune cells, and other cell types in the epidermis in response to injury, infection, or stress. These mediators orchestrate local inflammation by regulating immune cell recruitment, vascular changes, cellular proliferation, and tissue remodeling. While essential for skin defense and healing, dysregulation leads to chronic inflammatory skin diseases such as atopic dermatitis, psoriasis, and allergic reactions. The term lacks molecular specificity and does not correspond to a unique therapeutic target; rather, each mediator and its cognate receptor or signaling pathway may serve as an individual target for therapy[4][3][6][7][10]. For structured drug discovery or therapeutic targeting, it is necessary to specify the exact molecule (e.g., "Interleukin-1 beta", "Tumor necrosis factor alpha") or the relevant receptor (e.g., "Interleukin-4 receptor alpha")[10][4][7].
Blockade of cytokine/receptor interaction (e.g., anti-TNF, anti-IL-4Rα); Inhibition of inflammasome assembly/activity; Suppression of immune cell activation/differentiation
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