Pro-inflammatory cytokine signaling in skin

Pro-inflammatory cytokine signaling in the skin is a complex biological process involving a network of signaling proteins that regulate immune responses and inflammation within the cutaneous environment (Source: PubMed - PMID: 31644311). Key cytokines involved in this signaling include Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-17 (IL-17), and Interleukin-23 (IL-23), which are central to the pathogenesis of chronic inflammatory diseases like psoriasis (Source: StatPearls - Psoriasis). In conditions such as atopic dermatitis, the signaling is dominated by Th2-type cytokines like IL-4 and IL-13 (Source: JACI - Guttman-Yassky et al., 2018). These cytokines bind to specific cell-surface receptors, often activating the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway to alter gene expression in keratinocytes and immune cells (Source: Frontiers in Immunology - Solimani et al., 2019). Therapeutic strategies targeting this signaling include monoclonal antibodies that neutralize specific cytokines (e.g., adalimumab, secukinumab) and small molecule inhibitors that block intracellular signaling (e.g., tofacitinib). While highly effective, modulating these pathways can lead to safety concerns such as an increased risk of serious infections due to suppressed immune surveillance (Source: FDA - Prescribing Information for Biologics).

Other names

Cutaneous cytokine signalingSkin inflammatory cascadeInflammatory signaling in skinCutaneous inflammatory pathway

Modulation of the inflammatory response through the targeted inhibition of specific cytokines (e.g., TNF-alpha, IL-17, IL-23, IL-4/13) or their respective receptors, as well as the inhibition of downstream intracellular signaling transducers such as Janus kinases (JAKs) to reduce cutaneous inflammation.