Uveitis is a group of inflammations inside the eye that is the leading cause of predictable vision loss. It is normally limited by physical barriers such as blood-aqueous and blood-retinal, the local immunosuppressive environment, and systemic tolerance, including the immune bias of the anterior chamber. In the autoimmune form, genetic susceptibility (HLA class I/II and enzymes such as ERAP) lowers the threshold for autoreactive T-cell activity, leading to Th1/Th17 responses in the draining nodes and in the eye to cytokine cascades from microglia and macrophages. B-cells exacerbate injury by antigen presentation, cytokines, antibodies, and ectopic lymphoid structures. Autoinflammatory uveitis arises from dysregulated innate pathways, infectious from direct infection or reactivation, postinfectious from persistent antigen or molecular mimicry, and paraneoplastic from cross-reaction of antitumor immunity with retinal antigens. Treatment depends on the type: in the case of infection, first antimicrobial agents and then anti-inflammatory agents, in the case of autoimmune blockade of TNF and IL-6, in the case of auto-inflammatory IL-1. Tissue memory T-cells persist in remission and influence the risk of relapse.