Cutaneous inflammation

Cutaneous inflammation is the orchestrated immune response within the skin, triggered by infectious, allergenic, or internal stimuli. It involves resident skin cells (e.g., keratinocytes, Langerhans cells), infiltrating immune cells (mast cells, lymphocytes, neutrophils), cytokines (e.g., IL-1β, TNF-α, IL-4, IL-13), and pattern recognition receptors (e.g., TLRs) that recognize pathogens or damage and initiate signal transduction pathways. This leads to typical clinical signs: redness, swelling, heat, pain, and often skin barrier disruption (rash, scaly skin, blistering)[1][2][4][6]. While vital for protection and tissue repair, dysregulated or chronic cutaneous inflammation underlies many dermatological diseases such as atopic dermatitis, psoriasis, and contact dermatitis[5][7]. Therapeutic interventions focus on suppressing inflammatory pathways through corticosteroids, immunomodulators, cytokine blockers, and barrier-repair agents[5][2].

Other names

Skin inflammationDermatitisInflammatory skin disease (ISD)

Not applicable for the process; underlying drugs act via: - Inhibition of cytokine signaling - Immune cell suppression (e.g., corticosteroids) - Mast cell stabilization - Blockade of receptor function (e.g., monoclonal antibodies against IL-4Rα, TNF-α)