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The **IL‑17 signaling pathway**, centered around members of the interleukin 17 family (notably **interleukin 17A**, produced primarily by Th† cells), orchestrates key aspects of innate and adaptive immunity. Upon ligand binding at its heterodimeric receptor complex (**interleukin 17 receptor A/C**, mainly on epithelial cells/fibroblasts), it activates intracellular cascades including NF-kappaB, MAPKs, C/EBPs via adaptor proteins like ACT1. This leads to robust induction of pro-inflammatory cytokines/chemokines that recruit neutrophils and other immune effectors; it also stimulates antimicrobial peptide production critical for mucosal defense but can drive pathological inflammation when dysregulated. Aberrant activity contributes significantly to autoimmune disease pathogenesis—and thus several biologics have been developed against key nodes within this network for clinical use in autoimmunity and chronic inflammatory disorders.
Drugs targeting this system typically act by: — Neutralizing circulating interleukins such as IL‑17A/F to prevent their binding to receptors. — Blocking cell surface receptors like IL‑17RA to inhibit downstream pro-inflammatory signal transduction. This results in reduced chemokine/cytokine production and decreased immune cell recruitment/inflammatory response.
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