Inflammatory response in epidermis

The inflammatory response in the epidermis is a process involving the activation of immune pathways, signaling molecules, and cellular responses to injury or infection in the outermost layer of the skin[5][3]. Epidermal cells such as keratinocytes, along with innate immune cells (macrophages, dendritic cells, mast cells), recognize harmful stimuli through receptors (e.g., toll-like receptors), produce pro-inflammatory cytokines (such as TNF-α, IL-17, IFN-γ, IL-22), and activate downstream signaling leading to recruitment of additional immune cells and tissue changes[3][5][1]. This multifaceted response is central to the pathology of several inflammatory skin diseases and is the focus of research into new therapeutic targets, such as scavenger receptor class B type 1 (SR-B1), transcription factors (like IKZF1), and cytokine signaling pathways (TNF/TNFR, IL-17/IL-23, EGFR/STAT1)[1][2][3]. Because "inflammatory response in epidermis" is not a distinct molecule or receptor, it is not appropriate to list it as a drug target. However, understanding the involved pathways and regulators helps guide the development of targeted therapies for skin inflammation.