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The Interleukin-17 (IL-17) pathway is a critical signaling axis in the immune system, primarily responsible for mediating pro-inflammatory responses and host defense against extracellular pathogens [1.2.2, 1.3.1]. The pathway consists of six cytokine ligands (IL-17A to IL-17F) and five receptor subunits (IL-17RA to IL-17RE), which form various functional complexes to initiate downstream signaling [1.1.5, 1.2.3]. Upon binding to their receptors, these cytokines recruit the adapter protein Act1, which subsequently activates the NF-κB, MAPK, and C/EBP signaling pathways [1.1.3, 1.3.3]. This cascade leads to the production of chemokines, antimicrobial peptides, and matrix metalloproteinases that recruit neutrophils and promote tissue inflammation [1.3.1, 1.3.4]. While essential for clearing fungal and bacterial infections, dysregulation of the IL-17 pathway is a central driver of autoimmune diseases such as psoriasis, psoriatic arthritis, and ankylosing spondylitis [1.2.5, 1.3.3]. Therapeutic targeting of this pathway, primarily through monoclonal antibodies that neutralize IL-17A or block the IL-17RA receptor, has shown high efficacy in treating these conditions [1.2.1, 1.2.5]. However, such interventions are associated with specific safety concerns, including an increased risk of mucocutaneous candidiasis and the potential for exacerbating inflammatory bowel disease [1.2.1, 1.3.3]. Emerging research also explores the role of this pathway in cardiovascular disease and cancer, highlighting its broad biological impact [1.1.1, 1.3.2].
Neutralization of IL-17 cytokines (IL-17A, IL-17F) or blockade of the IL-17 receptor (IL-17RA) to inhibit downstream pro-inflammatory signaling.
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