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and others)

*Also known as melanin protein-induced uveitis (EMIU).

*Also known as melanin protein-induced uveitis (EMIU).

which prevents free egress of lymphocytes from the circulation into the ocular tissues.

Current knowledge postulates that most lymphocytes capable of recognizing tissue-specific antigens are eliminated by negative selection in the thymus during ontogeny. Those that escape deletion must be controlled in the periphery by other tolerance-inducing mechanisms, such as clonal anergy or deletion due to encounter with tissue-specific antigen in the absence of accessory signals, or active suppression by regulatory cells. It is unclear, however, to what extent any of these mechanisms are operative in the case of ocular antigens. The separation between the immune system and the eye occurs early in ontogeny, and although recent work shows that messenger RNA encoding some retinal antigens can be detected in the thymus by the sensitive method of polymerase chain reaction (PCR), detectable levels of retina] proteins are not readily demonstrable in the thymus. Antibodies and lymphocytes that recognize ocular antigens are detectable in the blood of healthy human and animal subjects who show no evidence of autoimmunity. This supports the notion that there is neither clonal deletion nor inactivation of these cells. Disruption of the blood-retinal barrier during trauma or inflammation can give access to lymphocytes, which are not tolerant, into the eye. Antigen may be presented either locally (major histocompatibility complex (MHC) class II-expressing cells are present in the inflamed eye) or peripherally (antigen which escapes under the conjunctiva will be drained into regional lymph nodes). How, then, is ocular nonaggression maintained? And what are the circumstances leading to its breakdown, resulting in autoimmune uveitis?

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