Abstract
Inflammation is self-regulated to preserve the functions in the eye, because the eye has immune privilege. At present, three major mechanisms prevail regarding the molecular mechanisms of immune privilege in the eye: there are (a) anatomical, cellular, and molecular barriers in the eye; (b) eye-derived immunological tolerance, the so-called anterior chamber-associated immune deviation; and (c) immune suppressive intraocular microenvironment. In this mini-review, the mechanisms of immune privilege that have been learned from ocular inflammation animal models, especially corneal transplantation, are described. The functions of new molecules on local immune regulation within the cornea are reviewed. Therapeutic strategies for restoring immune privilege are also introduced.
