IL-17 in ocular fibrosis: From molecular mechanisms to precision therapeutics

Pathological fibrosis is a major cause of irreversible vision loss, yet effective antifibrotic therapies remain limited. Emerging evidence implicates interleukin-17 (IL-17) as an important immunomodulatory contributor linking chronic inflammation with aberrant tissue remodeling in the eye. This review synthesizes current knowledge on the molecular mechanisms by which IL-17 participates in fibrogenic processes, including its interaction with transforming growth factor-β (TGF-β), facilitation of epithelial-mesenchymal transition, myofibroblast activation, and extracellular matrix deposition. Across a spectrum of ocular diseases-ranging from ocular surface disorders to glaucoma and retinal pathologies-IL-17 signaling appears most prominent during early inflammatory phases, whereas advanced fibrosis may become increasingly sustained by IL-17-independent profibrotic circuits. We further discuss emerging precision therapeutic strategies targeting the IL-17 axis, including bispecific anti-IL-17/VEGF agents and localized delivery approaches. A clearer understanding of the temporal and cellular context of IL-17 signaling may help identify optimal intervention windows to mitigate fibrotic progression and preserve visual function.