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T helper 17 (Th17)-related cytokines represent a group of pro-inflammatory signaling molecules primarily produced by Th17 cells, a distinct lineage of CD4+ T cells. The hallmark members of this group include Interleukin-17A (IL-17A), IL-17F, IL-21, and IL-22, while IL-23 is critically involved in the stabilization and expansion of the Th17 phenotype. These cytokines play a vital role in host defense against extracellular pathogens by recruiting neutrophils and inducing the production of antimicrobial peptides at mucosal surfaces. However, dysregulation of the Th17 pathway is a major driver of various autoimmune and chronic inflammatory diseases, including psoriasis, ankylosing spondylitis, and rheumatoid arthritis. Therapeutic strategies targeting these cytokines, particularly IL-17 and IL-23, have revolutionized the treatment of moderate-to-severe plaque psoriasis and related spondyloarthritides. While highly effective, inhibition of these pathways can increase susceptibility to certain infections, most notably Candida species, and requires careful monitoring in patients with a history of inflammatory bowel disease.
Monoclonal antibodies bind to and neutralize specific cytokines (such as IL-17A, IL-17F, or IL-23) or block their cognate receptors (such as IL-17RA) to inhibit downstream signaling pathways like JAK-STAT or NF-kappaB, thereby reducing chronic inflammation.
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