IL17RA is a transmembrane receptor localized to chromosome 22 that mediates interleukin-17 signaling in immune and barrier tissues 1. The receptor binds IL-17A and related cytokines produced by T helper 17 cells, activating NF-κB signaling and downstream inflammatory responses including increased production of IL-6, chemokines, and other pro-inflammatory cytokines. IL17RA is expressed broadly across tissues including synovial endothelium, chondrocytes, and fibroblasts, and plays roles in host defense against extracellular pathogens as well as in autoimmune and inflammatory pathology 23. Clinically, IL17RA dysfunction associates with immunodeficiency—loss-of-function mutations cause immunodeficiency 51, characterized by susceptibility to chr22 mucocutaneous candidiasis—while elevated IL-17 signaling contributes to multiple inflammatory diseases including ankylosing spondylitis, asthma, and hidradenitis suppurativa 4. In colorectal cancer, IL17RA shows context-dependent effects: low expression associates with worse prognosis in advanced disease, and IL17RA deletion in epithelial cells promotes metastasis through altered immune tolerance, whereas IL17RA in macrophages supports anti-tumor immunity 5. In pancreatic cancer, IL-17A from tumor-infiltrating CD8+ T cells drives IL17RA-dependent fibroblast activation that promotes tumor growth and correlates with poor survival 6. The monoclonal antibody brodalumab, which blocks IL17RA, has demonstrated efficacy in psoriasis, with clinical trials of IL-17 pathway inhibitors ongoing across multiple inflammatory conditions 7.