Inflammatory cytokine signaling pathway in skin cells (null)

The inflammatory cytokine signaling pathway in skin cells encompasses the complex network through which cytokines (such as IL-1, IL-4, IL-6, IL-13, IL-17, IL-21, IL-22, IFN-γ, and others) and their receptors mediate inflammatory responses, cell proliferation, and barrier functions in the skin. This pathway is central to the pathogenesis of diseases like psoriasis and atopic dermatitis, coordinating the activity of keratinocytes and immune cells via intracellular signaling cascades (mainly the JAK-STAT and NF-κB pathways)[1][2][3][4][5]. Dysregulation or overactivation leads to chronic inflammation and abnormal skin cell proliferation. While drugs targeting components of this pathway (such as cytokine-neutralizing antibodies or JAK inhibitors) have shown efficacy in treating inflammatory skin diseases, the pathway itself is too broad to be a single therapeutic target—it comprises numerous biological entities with overlapping and context-dependent roles[3][4][5][6]. If a specific cytokine, receptor, or downstream effector (such as "Interleukin-17 receptor A" or "Janus kinase 1") is under consideration, it would be necessary to specify this precise molecular target for structured drug discovery.

Other names

Inflammatory cytokine signaling in skinCytokine signaling pathway in epidermisSkin inflammatory cytokine signaling

Cytokine neutralization (antibodies blocking cytokines or their receptors); JAK-STAT pathway inhibition (JAK inhibitors); Modulation of downstream inflammatory signaling (e.g., NF-κB, MAPK)