ABSTRACT
Research of immunological phenomena unique to the eye has substantially contributed to the study of autoimmunity and its potential pathogenicity. The eye’s anatomy is unique and allows high levels of sequestration of certain tissues from the immune system. Consequently, certain ocular-specific molecules may function as autoimmunogens and provoke autoimmunity, a capacity that was noticed almost a century ago. In fact, the production of autoantibodies against lens proteins by Uhlenhuth in 1903 was the first successful demonstration that autoimmunity is feasible, in defiance of the “horror autotoxicus” concept of Paul Ehrlich (cited in Ref. 1,2). Shortly thereafter, in 1906, Hess and Romer demonstrated autoimmunogenicity of proteins from the eye’s posterior segment (cited in Ref. 2) and provided conceptual basis for Elschnig’s suggestion (3) that sympathetic ophthalmia is caused by an autoimmune process. Sympathetic ophthalmia, that offers the most conspicuous demonstration of a human disease with an autoimmune etiology, develops as a consequence to a penetrating injury to one eye and consists of severe inflammation in both the injured eye, as well as in the untraumatized fellow eye (see Section 8).
