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"Inflammatory pathways in skin disorders" is not a single molecule or receptor but refers collectively to the complex network of cellular and molecular signaling cascades that mediate immune responses and inflammation in cutaneous tissues. These include well-characterized axes such as the NF‑κB pathway, JAK/STAT signaling, Th1/Th2/Th17 cytokine networks, and intracellular trafficking processes affecting cell adhesion molecules like desmoglein‑1. Dysregulation of these interconnected systems underlies common inflammatory skin diseases including psoriasis (driven by IL‑23/IL‑17), atopic dermatitis (Th2-mediated), acne, rosacea, urticaria, systemic lupus erythematosus and others[1][2][3][4][6]. Therapeutic interventions do not target "the inflammatory pathway" per se but rather focus on key mediators—such as interleukins or their receptors—within these broader networks. (Mechanistically, drugs target specific molecules within these pathways rather than the pathway as a whole; examples include biologics targeting cytokines like IL‑17 or IL‑23[2]) (Mechanisms are specific to individual molecular targets within these pathways.) (Biomarkers are typically proteins or cytokines within these pathways—e.g., IL‑17A for psoriasis—but not the pathway itself[1][3]) (Safety concerns pertain to drugs targeting components of these pathways, such as immunosuppression with biologics[2]) Note: This entry is not a valid therapeutic target according to standard conventions. It describes an entire class of biological processes rather than an individual druggable entity such as a receptor or enzyme. For structured data purposes you should extract and list specific validated targets involved in cutaneous inflammation—for example “Interleukin 17A” for psoriasis—or refer to recent proteomic studies identifying novel protein targets like RARRES2 or SERPINC1 for particular conditions[1][3].
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