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Abstract
Uveitis is a group of diseases characterized by intraocular inflammation, of which
some are driven by autoinflammatory or autoimmune responses, such as Vogt-Koyanagi-Harada
disease, Behçet's disease, uveitis associated with spondyloarthritis, ocular sarcoidosis,
sympathetic ophthalmia and birdshot chorioretinopathy. These entities have various
clinical forms, but genetic and biomarker data suggest that they share a common molecular
basis, activation of the Interleukin (IL)-23/IL-17 pathway. Multiple factors including
genetic predisposition, various cytokine imbalances, infectious agents and gut alterations
are found to trigger an aberrant response of this pathway. The enhanced activity of
the IL-23/IL-17 pathway is committed to the expansion and pathogenicity of Th17 cells.
Evidence from animal models demonstrates that the development of pathogenic Th17 cells
is responsible for the induction of experimental autoimmune uveitis. Further findings
indicate that retinal pigment epithelium (RPE) cells may be a target of IL-17. IL-17
triggers downstream inflammatory cascades and causes dysfunction of RPE cells, which
may affect retinal barrier function and thereby promote intraocular inflammation.
Currently, several emerging drugs blocking the IL-23/IL-17 pathway have been assessed
for the treatment of uveitis in pilot studies. The purpose of this is to summarize
updated biological knowledge and preliminary clinical data, providing the rationale
for further development and evaluation of novel drugs targeting the IL-23/IL-17 pathway
in autoinflammatory and autoimmune uveitis. Future studies may focus on translational
medicine targeting the IL-23/IL-17 pathway for the improvement of diagnosis and treatment
of uveitis. In conclusion, activation of the IL-23/IL-17 pathway is a critical biological
event and can be an important target for the treatment of autoinflammatory and autoimmune
uveitis.