Immune privilege in the anterior chamber of the eye, no longer considered a laboratory curiosity, results from an active, if deviant, systemic immune response. The specific features of this response, termed Anterior Chamber Associated Immune Deviation (ACAID) include (a) suppressed delayed hypersensitivity, (b) preserved humoral immunity, and (c) primed cytotoxic T cell responses. Induction of ACAID by intraocular antigens depends upon unique characteristics of the anterior segment of the eye and of the spleen. Evidence from animal models is presented in support of the contention that ACAID is an evolutionary adaptation of the immune response designed to provide those types of immune protection for the eye that interfere with vision as little as possible. ACAID may also have been created for the purpose of avoiding harmful immune responses (autoimmune diseases) to unique molecules of the eye (such as retinal S antigen), which the immune system never learns to regard as "Self." Because of this adaptation, the eye and the host are vulnerable to those pathogens whose elimination is dependent upon delayed hypersensitivity, such as malignant tumors and herpes simplex virus-1. As we come to understand the cellular and molecular mechanisms responsible for ACAID, a new generation of therapeutic strategies may be envisioned for certain eye diseases which are now of enigmatic cause and submit poorly to conventional therapy.