Uveitis is a sight threatening intraocular inflammation accounting for approximately 10% of blindness
worldwide. On the basis of aetiology, disease can be classified as infectious or non-infectious; and by anatomical
localization of inflammation as anterior, posterior and panuveitis. Non-infectious uveitis is believed to be autoimmune
in nature with Th1 and Th17 cells being identified as the prominent effector cell types. Numerous animal
models of autoimmune uveitis were developed contributing to our understanding of this inflammatory condition.
The classical peptide-induced experimental autoimmune uveoretinitis (EAU) model resembles human posterior
uveitis due to the recurrent/relapsing nature of the disease; while the intraocular inflammation triggered by administration
of bacterial lipopolisaccharide (endotoxin-induced uveitis, EIU) mimics closely anterior uveitis. The clinical need for novel,
more targeted forms of anti-inflammatory therapy has emerged as currently available therapeutic strategies are associated with a number
of adverse effects and intolerance in patients. This review summarises knowledge about existing mouse models of uveitis, discusses
mechanisms driving intraocular inflammation and describes possible customised translational treatment strategies that can be potentially
used in the clinic to prevent blindness in patients.
Keywords: Uveitis, autoimmunity, inflammation, uveitogenic antigens, animal models, Th1, Th17.
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