IL17A is a key effector cytokine of innate and adaptive immunity that signals through the IL17RA-IL17RC heterodimeric receptor complex to activate NF-κB and MAPK pathways, ultimately driving transcription of cytokines, chemokines, antimicrobial peptides, and matrix metalloproteinases 1. As the signature cytokine of T-helper 17 cells, IL17A primarily promotes neutrophil activation and recruitment at infection sites, connecting T cell-mediated immunity with acute inflammation to combat extracellular bacteria and fungi 1. In epithelial tissues, IL17A regulates tight junction biogenesis and barrier integrity while inducing antimicrobial peptide production in keratinocytes, including chemokines CXCL1, CXCL2, and CXCL8 that amplify inflammatory responses 2. IL17A dysregulation associates with multiple pathologies: polymorphisms in IL17A correlate with early-onset coronary artery disease susceptibility and Fanconi anemia risk 34, while elevated IL17A drives psoriasis pathogenesis through keratinocyte-mediated epidermal hyperproliferation and neutrophilic infiltration 2. Clinically, IL17A antagonism via monoclonal antibodies (secukinumab, ixekizumab, vunakizumab, xeligekimab) provides unprecedented efficacy for moderate-to-severe plaque psoriasis, psoriatic arthritis, and ankylosing spondylitis 567.