IL17F is an effector cytokine of innate and adaptive immunity involved in antimicrobial defense and tissue integrity maintenance. It signals via IL17RA-IL17RC heterodimeric or IL17RC homodimeric receptor complexes, triggering TRAF6-mediated activation of NF-κB and MAPK pathways that lead to transcription of cytokines, chemokines, antimicrobial peptides, and matrix metalloproteinases. As a signature Th17 effector, IL17F primarily drives neutrophilic inflammation and host defense against extracellular bacteria and fungi 123. It stimulates antimicrobial β-defensins from epithelial cells and regulates intestinal microbiota composition. Recent evidence suggests IL17F has distinct regulatory mechanisms and cellular sources compared to IL17A in psoriatic disease, with preferential elevation of IL17F over IL17A and expression in distinct T cell populations 4. Dual inhibition of IL17A and IL17F with bimekizumab demonstrates superior efficacy to single-pathway blockade in moderate-to-severe plaque psoriasis, achieving complete skin clearance (PASI 100) in 67% of patients at week 48 compared to 46.2% with IL17A inhibition alone 5. Sonelokimab, a nanobody targeting both IL17A and IL17F, also showed dose-dependent efficacy with rapid onset 6. The primary adverse effect of dual IL17A/F inhibition is oral candidiasis, reflecting IL17F's role in antifungal immunity 57.