Uveitis is a diverse group of sight-threatening intraocular inflammatory diseases usually causing eye redness, pain, blurred vision, and sometimes blindness. Although the exact pathogenesis of uveitis is not yet clear, accumulating evidences have shown that an imbalanced regulation of immune responses caused by a combination of genetic and environmental factors are implicated in the pathogenesis of this disease. As critical regulators of inflammation, inflammasomes have been assumed to play a role in the pathogenesis of uveitis. Recent studies have reported the association between a number of genetic variants in inflammasome related genes (such as NLRP3, NLRP1, NLRC4 and AIM2) with increased risk to uveitis. Mounting evidence have shown an aberrant activation of the NLRP3 inflammasome in both uveitis patients and murine models of uveitis. Some studies explored the intervention of uveitis via modulating inflammasome activity in the eye. This review aims at summarizing the main findings of these studies, proposing the possible mechanism whereby inflammasomes affect the susceptibility to develop uveitis, and giving a perspective for future studies, which may further improve our understanding about the role of inflammasomes and related cytokines in the pathogenesis of uveitis, and may hopefully lead to new therapeutics by targeting inflammasomes.