The thesis is advanced that immune responses to intraocular antigens are unique and highly specialized. Anterior chamber-associated immune deviation (ACAID) is the term used to identify this specialized response, which consists of selectively impaired immunity of the delayed hypersensitivity (DH) type coexistent with intact humoral immunity and priming of cytotoxic T cell activity. Induction of T cell suppression, which is partly responsible for ACAID, interferes with expression of DH within the eye as well as systemically. It is proposed that the ability of the eye to make a compromise with the immune system and thereby arrange for the selective suppression of delayed hypersensitivity results from the need to avoid intraocular inflammatory reactions that are intense and productive of nonspecific "innocent bystander" injury. When reactions of this type occur within the eye, the visual axis is disrupted, and vision is destroyed. However, avoidance of DH may have deleterious consequences both for the eye and for the host. The impact of ACAID is discussed with regard to the distinctive patterns of ocular disease produced experimentally in mice by melanoma cells and by herpes simplex virus type 1.