Immune privilege in the anterior chamber of the eye

Since the 19th century, it has been recognized that the anterior chamber of the eye permits the prolonged, and sometimes permanent, survival of foreign tissue and tumor grafts. It was initially believed that the absence of patent lymphatics draining the interior of the eye prevented antigens from reaching regional lymphoid tissues. However, sequestration of intraocular antigens alone cannot account for ocular immune privilege, and a clear picture is now emerging that a constellation of anatomical, physiological, and dynamic immunoregulatory factors contribute to ocular immune privilege. Ocular fluids contain a potpourri of immunosuppressive and immunoregulatory factors that suppress T-cell proliferation and secretion of proinflammatory cytokines. The interior of the eye is decorated with Fas ligand (CD95L), which induces apoptosis of infiltrating inflammatory cells. Antigens introduced into the eye induce a unique immune deviation in which T_H1 responses, namely delayed-type hypersensitivity (DTH), are actively suppressed. Thus, ocular immune privilege is sustained by factors that suppress immune cell proliferation and purge immune cells that enter the eye and by a dynamic immunoregulatory process that suppresses antigen-specific DTH. Suppression of certain inflammatory responses is an important adaptation for preventing immune-mediated injury to ocular tissues that have little or no capacity to regenerate. Thus, immune privilege is a crucial adaptation for preserving vision.