Keratinocyte inflammatory signaling pathways

Keratinocyte inflammatory signaling pathways represent the integrated network of molecular cascades that govern the skin's response to injury, infection, and environmental stress (Pasparakis et al., 2014, Nature Reviews Immunology). As the primary cell type in the epidermis, keratinocytes function as active immune sentinels, initiating and amplifying inflammatory responses through the secretion of cytokines, chemokines, and antimicrobial peptides (Liu et al., 2017, Frontiers in Pharmacology). Central to these processes are the NF-kappaB, Mitogen-Activated Protein Kinase (MAPK), and Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT) pathways, which translate external stimuli into gene expression changes (Howell et al., 2019, JACI). In pathological states like psoriasis and atopic dermatitis, these pathways become chronically activated, leading to aberrant keratinocyte proliferation and the recruitment of T-cells and neutrophils (Guttman-Yassky & Krueger, 2017, JID). Modern dermatological therapies target specific components of these pathways, such as Janus kinases or interleukin receptors, to modulate the immune environment and restore epidermal barrier function.

Other names

Keratinocyte inflammationEpidermal inflammatory signalingKeratinocyte-mediated immune response

Inhibition of intracellular signaling molecules (e.g., JAK, PDE4) or extracellular neutralization of cytokines and their receptors (e.g., TNF-alpha, IL-17, IL-4R) to dampen the inflammatory cascade.