Epidermal inflammatory signaling

Epidermal inflammatory signaling refers to the integrated network of molecular pathways in keratinocytes and other resident skin cells that coordinate the inflammatory response to environmental and endogenous triggers (Pasparakis, 2009). Key components include the activation of pattern recognition receptors (PRRs) and cytokine receptors, which trigger downstream cascades such as the NF-κB, MAPK, and JAK-STAT pathways (Dainichi et al., 2018). These pathways drive the expression of antimicrobial peptides, chemokines, and cytokines that recruit and activate immune cells. Dysregulation of epidermal inflammatory signaling is a central driver in the pathogenesis of chronic skin conditions like psoriasis, atopic dermatitis, and hidradenitis suppurativa (Guttman-Yassky & Krueger, 2017). Modern therapeutic interventions target specific nodes within this network, such as IL-17, IL-23, or Janus kinases, to suppress pathological inflammation and restore the skin's barrier function. Understanding the crosstalk between keratinocytes and immune cells within these pathways remains a primary focus for developing next-generation dermatological therapies.

Other names

Keratinocyte inflammatory signalingEpidermal cytokine signalingSkin inflammatory cascadeEpidermal immune signaling

Inhibition of specific cytokines (e.g., TNF-α, IL-17, IL-23) or intracellular signaling molecules (e.g., JAKs, PDE4) that mediate the inflammatory response within the epidermal and dermal layers of the skin.