Epidermal keratinocyte inflammatory signaling pathways

Epidermal keratinocyte inflammatory signaling pathways represent the integrated network of molecular cascades that govern the skin's response to injury, infection, and environmental stress. Keratinocytes, the predominant cell type in the epidermis, function as active immune sentinels by expressing pattern recognition receptors (PRRs) that trigger pathways such as NF-kappaB, MAPK, and JAK/STAT upon activation (Nestle et al., 2009, NEJM). These signaling events culminate in the secretion of a diverse array of pro-inflammatory cytokines, chemokines, and antimicrobial peptides that coordinate the local and systemic immune response (Pasparakis, 2009, Nature Reviews Immunology). Chronic dysregulation of these pathways is central to the pathogenesis of inflammatory dermatoses, including psoriasis and atopic dermatitis, where a feed-forward loop between keratinocytes and T-cells sustains inflammation (Guttman-Yassky & Krueger, 2017, JACI). Modern therapeutic interventions target specific components of these pathways, such as Janus kinases or specific cytokine receptors, to dampen the inflammatory cascade and restore epidermal homeostasis (Bissonnette et al., 2016, JID). Because this entry describes a broad biological process rather than a single molecular entity, it is classified as a pathway rather than a discrete therapeutic target.

Other names

Keratinocyte inflammatory responseEpidermal immune signalingKeratinocyte-mediated inflammationKeratinocyte signaling cascades

Inhibition of intracellular signaling molecules (e.g., JAK1/2/3, NF-kappaB, MAPK) or neutralization of extracellular cytokines (e.g., IL-17A, TNF-alpha, IL-4, IL-13) to disrupt the pro-inflammatory feedback loop between keratinocytes and immune cells.